The wound environment as a regulator of fibroblast phenotype

Regan, Mark; Kirk, Stephen; Wasserkrug, Hannah L.; Barbul, Adrian

doi:10.1016/0022-4804(91)90022-e

Cited by 62 publications

(39 citation statements)

References 27 publications

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“…The fibroblasts in that study were obtained from uninjured skin in the arm, whereas in our study, they were obtained from acute wounds, and fibroblasts from wounds are known to be phenotypically different from those in uninjured skin. 37 In our study, the proliferation of wound fibroblasts decreased in patients with type 1 but not type 2 diabetes compared with nondiabetic controls. Fibroblasts are the main source of collagen, and the number of fibroblasts can be taken for a measure of repair.…”

Section: Commentmentioning

confidence: 73%

Decrease of Collagen Deposition in Wound Repair in Type 1 Diabetes Independent of Glycemic Control

Black¹

2003

Arch Surg

105

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Type 1 and type 2 diabetes mellitus and glycemic control influence wound healing in humans.Design: Experimental study using a human woundhealing model.Setting: Collaboration among a multidisciplinary woundhealing department, department of medicine, and research laboratories.Patients, Control Subjects, and Methods: In 34 patients with type 1 (insulin-dependent) and 25 with type 2 (non-insulin-dependent) diabetes and 5 nondiabetic control subjects matched with the type 2 diabetic patients, wound-healing capacity was determined as subcutaneous accumulation of collagen measured as hydroxyproline. Two expanded polytetrafluoroethylene tubes were implanted and removed 10 days later. The hydroxyproline level was determined by means of high-performance liquid chromatography; the collagenase activity, by using a radiolabeled collagen substrate. Proliferation of fibroblasts cultured from the wounds was studied in patient groups. Results:The deposition of hydroxyproline decreased by 40% (P=.03) in type 1 compared with type 2 diabetes (median, 0.70 vs 1.16 nmol/mg; interquartile range, 0.48-1.04 vs 0.56-1.63 nmol/mg), which in turn did not differ significantly from that of controls (median, 1.35 nmol/ mg; interquartile range, 0.72-1.88 nmol/mg). The decreased collagen deposition in type 1 diabetes was not caused by increased collagenase activity. The deposition of hydroxyproline did not correlate significantly (r s =0.07; P=.63) with glycosylated hemoglobin levels in either diabetic group. Fibroblast growth was also decreased in type 1 compared with type 2 diabetic patients and controls.Conclusions: Collagen deposition in acute wounds is impaired in type 1 diabetes, possibly due to a decreased fibroblast proliferation. In type 2 diabetes, collagen deposition is normal. Glycemic control does not influence collagen deposition in acute wound repair in type 1 or in type 2 diabetes mellitus.

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Section: Commentmentioning

confidence: 73%

Decrease of Collagen Deposition in Wound Repair in Type 1 Diabetes Independent of Glycemic Control

Black¹

2003

Arch Surg

105

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“…Wound fibroblasts (WF) were obtained from male Sprague-Dawley rats wounded as described previously [26]. Seven days after wounding the sponges were excised, cleared of surrounding granulation tissue, and incubated overnight in 30 mL of collagenase solution (200 U/mL; Sigma, St. Louis, MO) in Dulbecco's modified Eagle medium (DMEM) (Gibco, Carlsbad, CA ) at 37 C in a humidified atmosphere of 5% CO 2 .…”

Section: In Vitro Experimentsmentioning

confidence: 99%

Role of High Mobility Group Box 1 (HMGB1) in Wound Healing

Zhang

O’Hearn

Kavalukas

et al. 2012

Journal of Surgical Research

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“…Nicht nur das elastische Kollagen Typ III trägt in der initialen Phase zur Wundkontraktion bei, sondern auch der TGF-β 1 -gesteuerte Phänotypwechsel der Fibroblasten in sog. Myofibroblasten, die in der zytoskelletalen Struktur kontraktile Fasern enthalten [29]. Die rasch zunehmende Festigkeit der Anastomose während der proliferativen Phase geht im Wesentlichen auf die zunehmende Synthese des Kollagens Typ I mit den festeren Fibrillen zurück, obwohl sich im Anastomosenbereich weitere Kollagentypen in geringerer Konzentration finden [5].…”

Section: Kollagensyntheseunclassified

Physiologie der Anastomosenheilung

Marjanović

Hopt

2010

Chirurg

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Anastomotic insufficiency still remains the most dreaded complication following digestive surgery. The surgeon's understanding of the mechanisms underlying anastomotic healing and the possible weak points are just as important as a correct anastomotic technique. Intestinal anastomotic healing is a complex, cell-mediated process which aims at restoring bowel wall continuity. The early stages of anastomotic healing are most susceptible to various sources of irritation, which is reflected by the likelihood of early anastomotic insufficiency. In our opinion, the focus of future research should shift from primarily examining pathogenetic factors to a more cellular and molecular level. A better comprehension of the anastomotic healing process might thus promote the development of new diagnostic predictive and therapeutic methods.

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The wound environment as a regulator of fibroblast phenotype

Cited by 62 publications

References 27 publications

Decrease of Collagen Deposition in Wound Repair in Type 1 Diabetes Independent of Glycemic Control

Decrease of Collagen Deposition in Wound Repair in Type 1 Diabetes Independent of Glycemic Control

Role of High Mobility Group Box 1 (HMGB1) in Wound Healing

Physiologie der Anastomosenheilung

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