Exogenous TGF-beta stimulates the formation of granulation tissue which increases the rate of wound closure in full thickness skin wounds.  The chronic expression of TGF beta can stimulate the formation of scar tissue which can interfere with other kinds of wound healing, e.g. nerve re-growth in spinal cord injury.  As with most things related to TGFbeta, its action depends on the cellular and physiological context.

hello

The literature might have varied interpretation depending on how the experiment was performed. I have attached two papers on how they interpret the role of TGF-beta in wound healing. You can also prove the effect of TGF-beta on wound healing by performing wound healing assay. After the assay u can analyse your result by following this software called tscratch, which automatically does the calculation for you. it uses the initial wound created and wound closure during the expt to give you a measurement of how your treatment varies from the control. Please find attached the protocol for wound healing assay and the software for the analysis

cheers bro!!!!!!!!!!!

http://www.ncbi.nlm.nih.gov/pubmed/9076942

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415964/

http://www.nature.com/nprot/journal/v2/n2/full/nprot.2007.30.html

http://www.biotechniques.com/multimedia/archive/00045/BTN_A_000113083_O_45150a.pdf

Hi,

As Bruce mentioned, it depends a lot on context.So you might gain something by trying to be more speciifc. "Helping" with wound healing implies that there is "good" wound healing. Do you look at the time of closure of the wound? Or are you interested in reduced scarring? For medics this is often a trade-off. Also it depends on what you mean by wound healing. Scratch wound assays as Khamal suggests? Then you would usually only have one cell type (endothelial or fibroblastic?). Or full thickness skin wounds as Bruce mentioned? Then the species will matter.  Also note that there are different TGF-beta isoforms which act differently.

In any case the reviews posted by Khamal seem to be a good starting point.

Thank you All..

but my doubt is regarding these diabetic wound healing..

Is These TGF-beta will helpful only in wound contraction and in some literature shows it plays a main role in hypertrophic scarring..

if I use inhibitors for TGF-beta it will be helpful for diabetic wound healing?

Did those papers that report the role of TGF-beta only in wound contraction explicitly check for scarring? Many studies stop at the point of wound closure.Are you asking about a specific mouse model, or about humans? Again: What do you mean with "helpful"? Faster closure or less scarring? Or something else? According to the publication below TGF-beta1 is involved in both: faster closure through contraction AND increased hypertrophic scarring as two sides of the same medal.

Article The myofibroblast: Paradigm for a mechanically active cell

Iam asking about humans diabetic wound healing.

Helpful means faster wound healing in diabetic patients by inhoibiting TGF-beta

One of the main focuses of recent research has been the role played by the growth factor TGF-β in the process of both wound healing and scar formation. The three isoforms (TGF-β1, TGF-β2 and TGF-β3) appear to have overlapping functions and predominantly mediate their effects through the intracellular SMAD pathway. Initial research suggested that TGF-β1 was responsible for the fibrotic scarring response whereas the scarless wound healing seen in fetal wounds was due to increased levels of TGF-β3. However, the reality appears to be far more complex and it is unlikely that simply altering the ratio of TGF-β isoforms will lead to scarless wound healing. Other aspects of the TGF-β system that appear promising include the downstream mediator CTGF, the proteoglycan decorin and the binding protein p311.

TGFbeta, the ever bipolar growth factor. There are many things to consider but your question is concret. Diabetes induces TGFbeta signaling activation. But the problem is that you should inhibit TGFbeta partially cause in my experience TGFbeta strong blocking in open wounds induce secundary intention healing with strong fibrosis generation. Once the epidermis and basal membrane is recovered, cells interactions allow a TGFbeta inhibition with different effects. So, while wound is open TGFbeta inhibition is not recomended at least a total inhibition.

If you are considering a clinical trial of TGF-beta in diabetic skin ulcers......Been there, done that...got the T-shirt.  Contact me through LinkedIn if you would like more details.

Robson M, Steed D, McPherson JM, Pratt BM. and the TGF-b Study Group. 2002. Effects of TGF-b2 on wound healing in diabetic foot ulcers: A randomized controlled safety and dose-ranging trial. J Applied Res 2:133-145.