the Skeletal Muscle Differentiation CHOICE

[xtraflossy]

Ok, so I was checking this huge list I pout together months ago of possible "new toys" and decided to take another look at it. While looking up one of these, I came accross this study. While is will not satisfy you by suppling a final answer to the question of "What makes cells favor hyperplasia over hypertrophy?" , it does make fore a good, informative read to say the least.


LMD, while I know your working on another "thing" right now, Give this one 5 min.




Comparative Proteomes of the Proliferating C2C12 Myoblasts and Fully Differentiated Myotubes Reveal the Complexity of the Skeletal Muscle Differentiation Program*,S
......

. "PDQuest image analysis of the most abundant 2,139 proteins revealed that vast majority of these most likely represented gene products relegated to structural and/or housekeeping functions and apparently did not undergo major regulation. In contrast, expression of 75 polypeptides was consistently altered as mononucleated, proliferating C2C12 myoblast cells exited cell cycle and became MHC-positive, post-mitotic multi-nucleated myotubes. In addition, we identified 26 phospho-proteins that underwent differential expression during myogenic differentiation of C2C12 cells. Included among the differentially regulated proteins were mediators of inter- and intracellular signaling, cell shape, protein folding and stability, cell proliferation and apoptosis, and putative regulators of transcriptional and post-transcriptional modes of muscle-specific gene expression. We should note that although most of the differentially expressed proteins seen here are already known to be either directly or indirectly involved in myogenesis, a number of gene products (e.g. HSP90, transcription intermediary factor 1ß (TIF1ß) and IKB kinase subunit) with unprecedented involvement in skeletal muscle differentiation were also uncovered by our experiments."
http://www.mcponline.org/cgi/content/full/3/11/1065

 

[LakeMountD]

It says that undergo "myogenic differentiation". That isn't necessarily hyperplasia. It doesn't state hyperplasia anywhere in that article. Muscle cells are incapable of DNA synthesis, the process of splitting like say skin cells would, so instead they rely on differentiation (caused by our good friend IGF-1) of myoblasts (aka satellite cells, stem cells, or nuclei) that fuse to the damaged cells and can replace them. Hyperplasia is a very gray area right now for me, I have to do MUCH more research on it to fully understand it. And boy is it hard to find "trusted" studies on MUSCLE hyperplasia.

 

[xtraflossy]

Well, you kinda had to read into things a bit.

The study didn't say hyperplasia,.. this I know (and began by saying it doesnt answer the hyperplasia question) . It does say:
"Quantification of more than 2,000 proteins from C2C12 myoblasts and myotubes revealed that a vast majority of the abundant proteins appear to be relegated to the essential, housekeeping and structural functions, and their steady state levels remain relatively constant. In contrast, 75 proteins were highly regulated during the phenotypic conversion of rapidly dividing C2C12 myoblasts into fully differentiated, multi-nucleated, post-mitotic myotubes"
"We found that differential accumulation of 26 phospho-proteins also occurred during conversion of C2C12 myoblasts into myotubes"
The study (for me) was more of what alterations are made, and by what, that influence cell fate.
Differentieation of myoblasts
Translated in my head like this:
We have satalitte cells. These cells are located around muscle tissue. After loading, they aid in repair (fusion to damaged tissue)
Ok- so this study goes into chemical messengers and what alterations are made internally (aside from normal housekeeping) that will define what the cell does.

Knowing what alterations are specific to what fate could allow those alterations to be favored at will by other means...

 

[LakeMountD]

Well, you kinda had to read into things a bit.

The study didn't say hyperplasia,.. this I know (and began by saying it doesnt answer the hyperplasia question) . It does say:
"Quantification of more than 2,000 proteins from C2C12 myoblasts and myotubes revealed that a vast majority of the abundant proteins appear to be relegated to the essential, housekeeping and structural functions, and their steady state levels remain relatively constant. In contrast, 75 proteins were highly regulated during the phenotypic conversion of rapidly dividing C2C12 myoblasts into fully differentiated, multi-nucleated, post-mitotic myotubes"
"We found that differential accumulation of 26 phospho-proteins also occurred during conversion of C2C12 myoblasts into myotubes"
The study (for me) was more of what alterations are made, and by what, that influence cell fate.
Differentieation of myoblasts
Translated in my head like this:
We have satalitte cells. These cells are located around muscle tissue. After loading, they aid in repair (fusion to damaged tissue)
Ok- so this study goes into chemical messengers and what alterations are made internally (aside from normal housekeeping) that will define what the cell does.

Knowing what alterations are specific to what fate could allow those alterations to be favored at will by other means...

I mean don't get me wrong, this is a VERY detailed study but still only reveals hypertrophy. Doesn't really give any insight to hyperplasia from what I am seeing. The quote you have in there just refers to myoblasts (which are MONOnucleated satellite cells) are differentiated (fused and given a DNA to that of a myotube) into MULTI-nucleated post-mitotic tissue. Post-mitotic just refers to the process that takes place during differentiation.

If you want to look deeper into why some of this occurs do a search for IFBP-rP1, MyoD, and M-cadherin. That will give you a better idea of gene expression and what actually takes place. It is thought that IFBP-rP1 is the actual binding protein responsible for preventing differentiation of cells.

Although they don't mention MGF (probably because they didn't know enough about it at the time), this could be MGF's binding protein.

 

[xtraflossy]

I mean don't get me wrong, this is a VERY detailed study but still only reveals hypertrophy. Doesn't really give any insight to hyperplasia from what I am seeing. The quote you have in there just refers to myoblasts (which are MONOnucleated satellite cells) are differentiated (fused and given a DNA to that of a myotube) into MULTI-nucleated post-mitotic tissue. Post-mitotic just refers to the process that takes place during differentiation.

If you want to look deeper into why some of this occurs do a search for IFBP-rP1, MyoD, and M-cadherin. That will give you a better idea of gene expression and what actually takes place. It is thought that IFBP-rP1 is the actual binding protein responsible for preventing differentiation of cells.

Although they don't mention MGF (probably because they didn't know enough about it at the time), this could be MGF's binding protein.

Well, I liked the fact that this area was being explored,... shedding light onto the "controlling" areas of cell fate.

IFBP-rP1, what is that protein relted to? (Ill search of course, just my home pc is a little messed up, so i might not be able to)
Curious though,.. IF it IS responsable for diferentuation (sp) what would over expression do? Alow continuation of prolifferation?.. hmm. Ya know LMD- we sould write the "important" questions down so we can tell the researchers,...:icon_lol:

 

[LakeMountD]

Well, I liked the fact that this area was being explored,... shedding light onto the "controlling" areas of cell fate.

IFBP-rP1, what is that protein relted to? (Ill search of course, just my home pc is a little messed up, so i might not be able to)
Curious though,.. IF it IS responsable for diferentuation (sp) what would over expression do? Alow continuation of prolifferation?.. hmm. Ya know LMD- we sould write the "important" questions down so we can tell the researchers,...:icon_lol:

IFBP-rP1 was said to inhibit differentiation. It might have something to do with MGF. There is a specific article on it, just google it.