Focal adhesion kinase (FAK) siRNA inhibits human hypertrophic scar by suppressing integrin α, TGF‐β and α‐SMA. (24th April 2014)
- Record Type:
- Journal Article
- Title:
- Focal adhesion kinase (FAK) siRNA inhibits human hypertrophic scar by suppressing integrin α, TGF‐β and α‐SMA. (24th April 2014)
- Main Title:
- Focal adhesion kinase (FAK) siRNA inhibits human hypertrophic scar by suppressing integrin α, TGF‐β and α‐SMA
- Authors:
- Chen, Rui
Zhang, Zhiliang
Xue, Zhujia
Wang, Lin
Fu, Mingang
Lu, Yi
Bai, Ling
Zhang, Dongqing
Fan, Zhihong - Abstract:
- <abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10265-sec-0001" sec-type="section"> <p>The effect of focal adhesion kinase (FAK) on suppressing scarring and the potential molecular mechanism underlying it has been investigated. Ten samples of human hypertrophic scars (HS) tissue cultured in vitro were transfected with FAK siRNA mediated by liposome. Quantitative real‐time PCR was used to detect the expression of integrin α, transforming growth factor‐β (TGF‐β), FAK and α‐smooth muscle actin (α‐SMA) after transfection. MTT assay was used as a measure of fibroblast proliferation. Flow cytometry and <sup>3</sup>H‐proincorporation technique gave measurements of the cell cycle and the quantity of collagen synthesis, respectively. Expression of FAK was effectively blocked, accompanied by decreasing expression of integrin α, TGF‐β and α‐SMA in hypertrophic scars fibroblast (HSFB) cells. One to 4 h after transfection with FAK siRNA, proliferation of HSFB cells was strongly inhibited (<italic>P</italic> &lt; 0.01), reaching a maximum at 48 h. The proportion of G<sub>1</sub> cells was higher and the proportion of the S and G<sub>2</sub> cells lower after transfection. The amount of collagen synthesis in HSFB cells decreased when HSFB cells were transfected for 48 h. RNA interference targeting the FAK gene can block the two abnormal signal transduction pathways mediated by the integrin and TGF‐β receptors that are responsible for hyperplasia and<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10265-sec-0001" sec-type="section"> <p>The effect of focal adhesion kinase (FAK) on suppressing scarring and the potential molecular mechanism underlying it has been investigated. Ten samples of human hypertrophic scars (HS) tissue cultured in vitro were transfected with FAK siRNA mediated by liposome. Quantitative real‐time PCR was used to detect the expression of integrin α, transforming growth factor‐β (TGF‐β), FAK and α‐smooth muscle actin (α‐SMA) after transfection. MTT assay was used as a measure of fibroblast proliferation. Flow cytometry and <sup>3</sup>H‐proincorporation technique gave measurements of the cell cycle and the quantity of collagen synthesis, respectively. Expression of FAK was effectively blocked, accompanied by decreasing expression of integrin α, TGF‐β and α‐SMA in hypertrophic scars fibroblast (HSFB) cells. One to 4 h after transfection with FAK siRNA, proliferation of HSFB cells was strongly inhibited (<italic>P</italic> &lt; 0.01), reaching a maximum at 48 h. The proportion of G<sub>1</sub> cells was higher and the proportion of the S and G<sub>2</sub> cells lower after transfection. The amount of collagen synthesis in HSFB cells decreased when HSFB cells were transfected for 48 h. RNA interference targeting the FAK gene can block the two abnormal signal transduction pathways mediated by the integrin and TGF‐β receptors that are responsible for hyperplasia and contracture of the scar, making FAK iRNA therapy a potentially effective approach in HS treatment.</p> </sec> </abstract> … (more)
- Is Part Of:
- Cell biology international. Volume 38:Number 7(2014)
- Journal:
- Cell biology international
- Issue:
- Volume 38:Number 7(2014)
- Issue Display:
- Volume 38, Issue 7 (2014)
- Year:
- 2014
- Volume:
- 38
- Issue:
- 7
- Issue Sort Value:
- 2014-0038-0007-0000
- Page Start:
- 803
- Page End:
- 808
- Publication Date:
- 2014-04-24
- Subjects:
- Cytology -- Periodicals
Cells -- Periodicals
571.605 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1095-8355 ↗
http://www.cellbiolint.org/cbi/default.htm ↗
http://www.sciencedirect.com/science/journal/10656995 ↗
http://onlinelibrary.wiley.com/ ↗
http://firstsearch.oclc.org ↗ - DOI:
- 10.1002/cbin.10265 ↗
- Languages:
- English
- ISSNs:
- 1065-6995
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3097.707000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3661.xml