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(Bio) Cells: Potentially Harmful 'Undead Cells'

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PostPosted: Sat Feb 04, 2006 10:10 am    Post subject: (Bio) Cells: Potentially Harmful 'Undead Cells' Reply with quote

Potentially Harmful 'Undead Cells' Collect with Age
By Bjorn Carey
LiveScience Staff Writer
posted: 02 February 2006
02:00 pm ET

As you age, so do your cells. A new study reveals that old cells make up a much larger portion of skin cells than previously thought.

Over the years, cells lose the ability to divide and they enter a state called senescence. They're not dead, but they're not quite functioning correctly either. These undead cells may delay wound healing, weaken immune responses, and help cause wrinkles.

"Senescence is not cell death, and that's really the problem with it," said John Sedivy of Brown University.

'Scary number'

Earlier studies suggested that senescent cells made up only a few tenths of a percent of living organisms. This study, performed on baboons, indicates that the amount could be as much as 20 percent in the elderly. Baboons and humans are very similar on a cellular level, so these findings likely hold true for us as well, the scientists figure.

"Twenty percent is a scary number in aged skin," Sedivy told LiveScience. "It means that 20 percent of your skin cells are nonfunctional and could be harmful."

Senescent cells have been extensively studied in tissue culture dishes, but this study, published online today by the journal Science, is the first to show that they're present in substantial amounts in living organisms.

To count the number of senescent skin cells at different life stages, researchers took small skin samples from the forearms of baboons living on a research preserve. The primates ranged from 5 to 30 years, roughly equivalent to ages 15 to 90 in humans.

Sedivy and his team tested the sample cells for certain biomarkers that indicate cellular aging. They found that the number of senescent cells increased exponentially with age. In 5-year-olds they made up only 4 percent of the sample cells; in 30-year-olds the figure increased to 20 percent.

Hanging around

For some reason, the body doesn't actively remove these cells and they accumulate over the course of an organism's life.

"They basically hang around and don't do anything, and that in itself could be deleterious," Sedivy said. "If they're not functioning normally, and just sitting there taking up space, that could damage surrounding cells."

Other evidence, Sedivy said, suggests that they might actively secrete chemicals that harm surrounding tissue.

The body removes other types of old, broken down cells. So why not these?

Most likely it's because most advantageous traits, crafted from thousands of years of evolution, are meant for healthy, reproductive individuals. Once that stage of life has passed, the body doesn't care what happens and damaging, cancerous cells are allowed to run amok, the researchers figure.

In the case of wild baboons, these cells never get the chance to hang around so long. Once a baboon passes the reproductive age, it is usually killed by a younger, more virile animal.


Questions to explore further this topic:

What are cells?

Viewing cells

How can we study cells?

What are the different types of cells?

What are the parts of a cell?

How do cells work?

Types of cells in the blood

Nerve cells

What are stem cells?

How do cells reproduce?

Why do we age?

How do cells age and die?


Last edited by adedios on Sat Jan 27, 2007 3:35 pm; edited 2 times in total
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PostPosted: Fri Oct 20, 2006 9:57 am    Post subject: Scientists prove that parts of cell nuclei are not random Reply with quote

Imperial College London
19 October 2006

Scientists prove that parts of cell nuclei are not arranged at random

The nucleus of a mammal cell is made up of component parts arranged in a pattern which can be predicted statistically, says new research published today. Scientists hope this discovery that parts of the inside of a cell nucleus are not arranged at random will give greater insight into how cells work and could eventually lead to a greater understanding of how they become dysfunctional in diseases like cancer.

The study, published today in PLoS Computational Biology, involved systems biologists working together with mathematicians to identify, for the first time, 'spatial relationships' governing the distribution of an important control protein in the nucleus, in relation to other components within the nuclei of mammal cells.

This widespread protein called CBP acts on certain genes within the cell nucleus, turning them on to make specific proteins at different times throughout the life of the cell. The research began with a team of biologists in Canada labelling components inside cell nuclei with fluorescent dyes, which enabled them to identify concentrated pockets of CBP. However the pattern seen under the microscope is very complex. When the 'nearest neighbours' of the CPB pockets, such as gene regions and other protein machinery are visualised, the spatial relationships become too difficult to define.

To overcome this, the mathematicians involved in the research analysed the nearest neighbour distance measurements between the nuclei's components, and developed a toolkit for showing where other proteins and gene regions are likely to be located in relation to CBP across the nucleus. Specifically, they were able to develop a model for showing which components were more likely to be located closest to a CBP pocket, and those that were less likely. This effectively created a probability map of the nucleus, with components' locations derived relative to the location of concentrations of CBP.

Professor Paul Freemont from Imperial College London's Division of Molecular Biosciences one of the leaders of the research said: "We chose to focus on CBP because it is a well established gene regulator that activates genes by altering their local structure to allow the production of the specific proteins encoded by the genes. By using fluorescent dyes and sophisticated imaging techniques, we discovered that CBP pockets are more likely to be located closest to gene regions with which it is known to modify. This research is very important as it advances our understanding of how the cell nucleus is organised, although it leaves us with a 'chicken-or-egg' question to answer: is CBP located close to certain gene regions because they are active or does the location of CBP result in the activation of these genes?"

By developing these quantitative approaches and applying them more broadly, biologists will in the future be able to have complete spatial models for cells that not only define where things are but also the likelihood of them being in a particular location at a particular time. This will allow a deeper understanding of how cells are organised and will be of particular importance in understanding and predicting cells whose structure becomes altered as a first sign of disease such as cancer.

Professor Freemont added: "This research is groundbreaking in the field of systems biology because we're working with mathematicians to provide a solid statistical framework to explain aspects of how the cell nucleus is organised."
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PostPosted: Fri Mar 09, 2007 8:16 am    Post subject: Location, location -- Cell sizes, lives influenced by host s Reply with quote

University of Florida
8 Marchg 2007

Location, location -- Cell sizes, lives influenced by host size

Species' sizes affect lives of cells in mammals
Cells from the smallest to the largest of mammals often seem to be "one size fits all." Now a closer look reveals that whether a cell lives in an elephant, mouse or something in between can make a big difference in its life.

Researchers from the University of Florida Genetics Institute, Harvard Medical School and other institutions developed mathematical models that they used to examine 18 cell types from mammals ranging from mice to elephants. They found two basic categories — cells that stay the same size but have drastically different energy needs that depend on the size of the mammal, or cells that grow larger in larger mammals and use energy at the same rate, no matter the mammal’s size.

The discovery, published online this month in the Proceedings of the National Academy of Sciences, begins to answer questions about how the size of an organism helps determine the life span of its cells, a finding that could help cell biologists and physiologists understand cell and organ function and their relation to disease.

"Although cells are basic building blocks, their metabolic rates depend on where they find themselves living," said Van M. Savage, Ph.D., the lead author of the research and an instructor in the department of systems biology at Harvard Medical School. "Conceptually this is important because huge amounts of research on human diseases are done on single cells or cultured cells that come from other animals and little is done to place these findings within the context of the size or other whole-body properties of the animals."

Generally, the size of a species of mammal sets the pace of its life, Savage said. The life spans of a mouse and elephant can differ by more than 70 years, and it takes a mouse 20 days of gestation before delivering a baby compared with more than 600 days for an elephant. The larger the animal, the slower its cellular metabolic rate — the speed at which it burns oxygen — and life processes.

The question of whether cells are bigger in larger mammals than in smaller ones — think of an elephant’s liver cell compared with a liver cell from a mouse — is usually answered by saying that larger mammals don’t typically have bigger cells, they just have more of them.

Liver cells, red blood cells and other cell types that frequently divide and replace themselves are about the same size, but more permanent, long-lived cells, such as brain and fat cells, are indeed larger in large mammals.

"Fat cells increase in size tremendously if you move from a mouse to an elephant," said James Gillooly, Ph.D., an assistant professor in the zoology department of UF’s College of Liberal Arts and Sciences. "Neurons also increase in size. But red blood cells are the same size whether they are in a mouse or an elephant. The reason brain and fat cells grow bigger could be because they live longer and have important long-term functions. In these cases, the properties of the cell are linked to the whole organism. But the sizes of quickly dividing cells are independent of the organism."

Neurons are essential parts of brain networks that retain memory, the researchers said, while fat cells are storehouses of energy that are vital for an animal’s survival when food supplies are short. As such, they are too valuable and would require a great deal of energy to be continually used and replenished in the body.

Scientists from the Santa Fe Institute, the Los Alamos National Laboratory, the National Center for Ecological Analysis and Synthesis and the University of New Mexico also participated in the study.

"The authors are saying cell size, body size and life span all go together," said Samuel Wang, Ph.D., an associate professor of molecular biology and neuroscience at Princeton University who was not a member of the research team. "In the case of brains, this suggests a reason having little to do with information processing for why bigger brains have more complex neurons than small ones. Instead of saying neurons are larger because of demands for information processing, it suggests information processing might be constrained by the fact that neurons are larger. But it doesn't answer why different neurons get bigger to different extents, so there is still a lot of room to develop answers about why neurons scale up the way they do."

More study is needed to understand the interplay between an organism and its cells, scientists say.

"Despite the progress that has been made in cell biology, we still have a relatively poor understanding about general characteristics of cells across species," Savage said. "The focus has been on how cells affect the whole organism, not on how the size of the organism and its energy requirements affect the cells."
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PostPosted: Wed Apr 25, 2007 9:37 am    Post subject: Asymmetry due to Perfect Balance Reply with quote

Asymmetry due to Perfect Balance
April 25th, 2007
Max Planck Institute of Biochemistry, Martinsried

Mathematical model allows elucidation of universal principles in cell polarity

Cell membranes are like two-dimensional fluids whose molecules are distributed evenly through lateral diffusion. But many important cellular processes depend on cortical polarity, the locally elevated concentration of specific membrane proteins. Roland Wedlich-Soldner at the Max Planck Institute of Biochemistry in Martinsried, Germany, and his colleagues at Harvard Medical School, Boston, The Stowers Institute for Medical Research, Kansas City, and the University of Texas Southwestern Medical Center, Dallas, have analysed and quantified how cortical polarity develops and how an asymmetric distribution of molecules can be dynamically maintained. In their study they combined experiments on living cells with a mathematical model to show among other things that polarised regions in membranes are defined with nearly optimal precision. This novel approach is an important step towards a spatially and temporally quantifiable model of the cell. (Cell, April 19, 2007)

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PostPosted: Thu Jun 21, 2007 7:29 am    Post subject: Surprising origin of cell's internal highways Reply with quote

Vanderbilt University Medical Center
20 June 2007

Surprising origin of cell's internal highways

Scientists have long thought that microtubules, part of the microscopic scaffolding that the cell uses to move things around in order to hold its shape and divide, originated from a tiny structure near the nucleus, called the centrosome.

Now, researchers at Vanderbilt University Medical Center reveal a surprising new origin for these cellular "highways." In the June issue of Developmental Cell, Irina Kaverina, Ph.D., and colleagues report that the Golgi apparatus -- a stack of pancake-shaped compartments that sorts and ships proteins out to their cellular destinations -- is the source of a particular subset of these microscopic fibers. The findings point to a novel cellular mechanism that may guide cell movement and possibly cancer cell invasion.

Microtubules are the largest of the three main types of filaments that make up the cytoskeleton -- a web of microscopic fibers inside the cell.

They form when two globular proteins, alpha- and beta-tubulin, polymerize into long chains, which then assemble into long, hollow tubes. In order to gain a foothold, nascent microtubule "seeds" must be anchored at a structure near the cell's nucleus called the centrosome or microtubule-organizing center (MTOC).

From the MTOC, the growing microtubules launch out in all directions to the cell's periphery. Their rapid assembly and disassembly helps transport proteins throughout the cell and generate polarized (directional) signal distribution that causes cells to move.

While microtubules in some specialized cells can originate from non-centrosomal structures, the centrosome has been considered the main origination point for microtubule "nucleation" in most cells. Until now.

"I've seen that there are lots of microtubules not attached to the centrosome," said Kaverina, assistant professor of Cell and Developmental Biology and senior author on the paper. "So I am trying to look at their origins."

The Golgi has been suspected to function as an MTOC, explained Kaverina. However, conclusively demonstrating this was impossible before the advent of live-cell imaging techniques that could reveal the true origins of these structures.

"The Golgi apparatus is very close to the centrosome," said Kaverina. "So if you're not looking at it precisely, it is hard to distinguish between the centrosome and Golgi."

To get a close look, Kaverina and colleagues tagged the growing ("plus") ends of microtubules in human retinal epithelial cells with a fluorescent molecule, videotaped their growth and carefully followed the tracks back to their origin.

"We show that not only the centrosome, but the Golgi also makes microtubules," Kaverina said. "And unlike centrosomal microtubules, which are radial and symmetric, these microtubules are directional."

They found that microtubules originating at the Golgi are directed toward the cell "front," or the leading edge, of motile cells. Since such an orientation is needed for directional migration, Kaverina hypothesizes that this subset of microtubules may influence cell motility by facilitating the transport of proteins needed for movement to the cell front.

"This new microtubule subset that we discovered directly connects the Golgi to the cell front, so it would be very logical if these microtubules act as ‘tracks' for this delivery," she said.

In addition to identifying this novel site of microtubule nucleation, Kaverina and colleagues also examined the molecular mechanisms governing the process. They found that proteins normally associated with the plus ends of microtubules, called CLASPs, localize to a specific compartment of the Golgi (the Trans Golgi Network) and stabilize the microtubule "seeds" at the Golgi.

Golgi-originating microtubules could also be an important factor influencing how cancer cells invade distant tissues.

Because microtubules play a central role in cell division, cancer drugs like colchicine, vincristine and paclitaxel (Taxol) can block cell division by altering microtubule dynamics.

"Many classic chemotherapy strategies affect microtubules, although it's not quite clear how these drugs influence cancer cells differently than normal cells," said Kaverina. "Both microtubule regulation of proliferation and microtubule regulation of migration and invasion probably contribute to the therapeutic effects."

Therefore, further study of this new subset of microtubules might offer insight into how the invasion of cancer cells into surrounding tissues could be halted.

The research was supported by the department of Cell and Developmental Biology at Vanderbilt University Medical Center, and grants from the Austrian Science Fund, Fundação para a Ciência e a Tecnologia of Portugal, Luso-American Foundation for Development Work, and the National Institutes of Health.

Contributing authors included Andrey Efimov, Ph.D., Nadia Efimova, and Paul Miller from Vanderbilt, and colleagues from the Austrian Academy of Sciences, New York State Department of Health, University of Melbourne (Australia), Erasmus Medical Center (Netherlands), University of Porto (Portugal), and Scripps Research Institute.
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PostPosted: Tue Jul 03, 2007 9:20 am    Post subject: Marine worm opens new window on early cell development Reply with quote

University of Oregon
2 July 2007

Marine worm opens new window on early cell development
Oregon researchers find ancient genetic mechanism guiding cell diversity -- one with ties to cancer

University of Oregon biologists studying a common ocean-dwelling worm have uncovered potentially fundamental insights into the evolutionary origin of genetic mechanisms, which when compromised in humans play a role in many forms of cancer.

Their research, appearing in the July issue of the journal Developmental Cell, also increases the visibility of a three-year effort at the UO to promote use of the bristle worm Platynereis dumerilii as a model organism for the study of evolutionary origins of cell types and animal forms.

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PostPosted: Fri Aug 10, 2007 2:11 pm    Post subject: New, more direct pathways from outside the cell-to-cell nucl Reply with quote

National Science Foundation
10 August 2007

New, more direct pathways from outside the cell-to-cell nuclei discovered

Material outside of a cell can move into cell nucleus more easily than previously believed
A team of Brooklyn College researchers has shattered a long-held belief that no direct pathway exists between material outside of a cell and the cell nucleus. (The cell is the smallest metabolically functional unit of life.)

It was already known that material outside of a cell can migrate into a cell. This occurs through processes known as endocytosis and phagocytosis, in which extracellular material is captured by a pinched-in segment of the cell membrane. This extracellular material then becomes trapped inside the resulting membrane-bound intracellular compartment, which is known as an endosome or phagosome.

It was also already known that material can migrate out of an endosome or phagosome and eventually enter the cell nucleus. But the Brooklyn College team has discovered that a phagosome and its contents can enter the cell's nucleus, where genetic information is stored and processed.

The team's discovery of the existence of direct pathways between extracellular material and cell nuclei will be published on August 10, 2007 in Cell Motility and the Cytoskeleton. The team was led by Ray Gavin and funded by the National Science Foundation (NSF).

Gavin says that these newly discovered direct pathways mean that "internalized material does not necessarily have to exit the phagosome before entering the nucleus." Therefore, his discovery means that "one less step is needed for extracellular material to get into the nucleus, and so it is far easier than previously thought for this material to get into the nucleus."

Eve Barak, an NSF program director, describes Gavin's discovery as "an amazing and potentially paradigm-changing observation," and predicts that it "will have an enormous impact on how scientists think about how cellular functions are regulated."

Gavin has only observed direct pathways from the extracellular environment to the nucleus in the one-celled protozoan Tetrahymena thermophila. But Gavin says that "other discoveries that were based on this protozoan were later shown to be almost global in their occurrence in the biological world." Therefore, these direct pathways may operate in other organisms as well.

The discovery of the pathways in the protozoan resulted from an observation made by Gavin about 10 years ago while simply watching cells through a microscope. "I am a patient and constant observer of living things," he says. "And I watch them all the time with no agenda in mind. Some people are window gazers. They stand in front of the window and just look. I do the same with cells."

During one of Gavin's agenda-less cell-watching sessions, he noticed phagosomes clustered around a cell's nucleus. "It made me wonder why the phagosomes were positioned in that way," Gavin said. Thereafter, Gavin periodically looked for this intriguing behavior again, and occasionally glimpsed it again.

But Gavin remained unable to systematically search for phagosome clusters around nuclei until he received NSF funding in 2006 to purchase a confocal microscope, which provides three dimensional views of the cell. Just like a person would eventually find a worm hidden in an apple by repeatedly slicing through the apple, Gavin found the intruiging phagosome behavior he sought by using the confocal microscope to repeatedly obtain views that sliced clear through the cell.

Specifically, the team tracked phagosomes carry extracellular material into the cell nuceli by introducing fluorescent latex beads into the area outside of the cell. They then observed the cells phagocytose (eat) the beads, which gradually moved to the nucleus. The arrival of the phagosomes and their loads at the nucleus was marked by the illumination of the nucleus by the beads. Similarly, the researchers also labeled the cellular membrane with a fluorescent dye, and then observed the pinched off, internalized membrane move to the nucleus.

"Biologists may now study the kinds of external molecules that can gain entry to the nucleus through these newly defined pathways and how these materials influence the nucleic material and its processes," said Gavin.

The National Science Foundation (NSF) is an independent federal agency that supports fundamental research and education across all fields of science and engineering, with an annual budget of $5.58 billion. NSF funds reach all 50 states through grants to nearly 1,700 universities and institutions. Each year, NSF receives about 40,000 competitive requests for funding, and makes nearly 10,000 new funding awards. The NSF also awards over $400 million in professional and service contracts yearly.

Receive official NSF news electronically through the e-mail delivery and notification system, MyNSF (formerly the Custom News Service). To subscribe, visit and fill in the information under "new users".

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PostPosted: Sun Aug 12, 2007 1:00 pm    Post subject: MIT creates 3-D images of living cell Reply with quote

Massachusetts Institute of Technology
12 AUgust 2007

MIT creates 3-D images of living cell

Method is similar to medical CT scans
CAMBRIDGE, MA - A new imaging technique developed at MIT has allowed scientists to create the first 3D images of a living cell, using a method similar to the X-ray CT scans doctors use to see inside the body.

The technique, described in a paper published in the Aug. 12 online edition of Nature Methods, could be used to produce the most detailed images yet of what goes on inside a living cell without the help of fluorescent markers or other externally added contrast agents, said Michael Feld, director of MIT's George R. Harrison Spectroscopy Laboratory and a professor of physics.

“Accomplishing this has been my dream, and a goal of our laboratory, for several years,” said Feld, senior author of the paper. “For the first time the functional activities of living cells can be studied in their native state.”

Using the new technique, his team has created three-dimensional images of cervical cancer cells, showing internal cell structures. They've also imaged C. elegans, a small worm, as well as several other cell types.

The researchers based their technique on the same concept used to create three-dimensional CT (computed tomography) images of the human body, which allow doctors to diagnose and treat medical conditions. CT images are generated by combining a series of two-dimensional X-ray images taken as the X-ray source rotates around the object.

“You can reconstruct a 3D representation of an object from multiple images taken from multiple directions,” said Wonshik Choi, lead author of the paper and a Spectroscopy Laboratory postdoctoral associate.

Cells don't absorb much visible light, so the researchers instead created their images by taking advantage of a property known as refractive index. Every material has a well-defined refractive index, which is a measure of how much the speed of light is reduced as it passes through the material. The higher the index, the slower the light travels.

The researchers made their measurements using a technique known as interferometry, in which a light wave passing through a cell is compared with a reference wave that doesn't pass through it. A 2D image containing information about refractive index is thus obtained.

To create a 3D image, the researchers combined 100 two-dimensional images taken from different angles. The resulting images are essentially 3D maps of the refractive index of the cell's organelles. The entire process took about 10 seconds, but the researchers recently reduced this time to 0.1 seconds.

The team's image of a cervical cancer cell reveals the cell nucleus, the nucleolus and a number of smaller organelles in the cytoplasm. The researchers are currently in the process of better characterizing these organelles by combining the technique with fluorescence microscopy and other techniques.

“One key advantage of the new technique is that it can be used to study live cells without any preparation,” said Kamran Badizadegan, principal research scientist in the Spectroscopy Laboratory and assistant professor of pathology at Harvard Medical School, and one of the authors of the paper. With essentially all other 3D imaging techniques, the samples must be fixed with chemicals, frozen, stained with dyes, metallized or otherwise processed to provide detailed structural information.

“When you fix the cells, you can't look at their movements, and when you add external contrast agents you can never be sure that you haven't somehow interfered with normal cellular function,” said Badizadegan.

The current resolution of the new technique is about 500 nanometers, or billionths of a meter, but the team is working on improving the resolution. “We are confident that we can attain 150 nanometers, and perhaps higher resolution is possible,” Feld said. “We expect this new technique to serve as a complement to electron microscopy, which has a resolution of approximately 10 nanometers.”

Other authors on the paper are Christopher Fang-Yen, a former postdoctoral associate; graduate students Seungeun Oh and Niyom Lue; and Ramachandra Dasari, principal research scientist at the Spectroscopy Laboratory.

The research was conducted at MIT's Laser Biomedical Research Center and funded by the National Institutes of Health and Hamamatsu Corporation.
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