Effect of prostaglandins on protein, RNA, DNA and collagen synthesis in experimental wounds

Lupulescu, A.

doi:10.1016/s0090-6980(75)80003-7

Cited by 45 publications

(14 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxidative stress due to hyperglycaemia caused by diabetes increases secretion of various cytokines, which induce COX-2, a modulator of the inflammatory response in the biosynthesis of prostaglandins. Over-expression of the COX-2 protein decreases collagen synthesis and retards proliferation, thus delaying the entire cutaneous wound healing [32]. We found that COX-2 expression levels in the DM group gradually increased, which may prolong the inflammatory responses and delay wound healing.…”

Section: Discussionmentioning

confidence: 93%

Short term supplementation of dietary antioxidants selectively regulates the inflammatory responses during early cutaneous wound healing in diabetic mice

Park

Lim

2011

Nutr Metab (Lond)

View full text Add to dashboard Cite

BackgroundDiabetic foot ulcers are serious complications for diabetic patients, yet the precise mechanism that underlines the treatment of these diabetic complications remains unclear. We hypothesized that dietary antioxidant supplementation with vitamin C, combined either with vitamin E or with vitamin E and NAC, improves delayed wound healing through modulation of blood glucose levels, oxidative stress, and inflammatory response.MethodsDiabetes was induced by administration of alloxan monohydrate. Mice were divided into 4 groups; CON (non-diabetic control mice fed AIN 93 G purified rodent diet), DM (diabetic mice fed AIN 93 G purified rodent diet), VCE (diabetic mice fed 0.5% vitamin C and 0.5% vitamin E supplemented diet), and Comb (diabetic mice fed 0.5% vitamin C, 0.5% vitamin E, and 2.5% NAC supplemented diet). After 10 days of dietary antioxidant supplementation, cutaneous full-thickness excisional wounds were performed, and the rate of wound closure was examined. TBARS as lipid peroxidation products and vitamin E levels were measured in the liver. Expression levels of oxidative stress and inflammatory response related proteins were measured in the cutaneous wound site.ResultsDietary antioxidant supplementation improved blood glucose levels and wound closure rate and increased liver vitamin E, but not liver TBARS levels in the diabetic mice as compared to those of the CON. In addition, dietary antioxidant supplementation modulated the expression levels of pIκBα, HO-1, CuZnSOD, iNOS and COX-2 proteins in the diabetic mice.ConclusionsThese findings demonstrated that delayed wound healing is associated with an inflammatory response induced by hyperglycaemia, and suggests that dietary antioxidant supplementation may have beneficial effects on wound healing through selective modulation of blood glucose levels, oxidative stress, and inflammatory response.

show abstract

Section: Discussionmentioning

confidence: 93%

Short term supplementation of dietary antioxidants selectively regulates the inflammatory responses during early cutaneous wound healing in diabetic mice

Park

Lim

2011

Nutr Metab (Lond)

View full text Add to dashboard Cite

show abstract

“…Certainly, since many other factors than luminal contents promote and retard the healing process of mucosal injury [17], and as prostaglandins have a variety of other actions, i.e. an increase in mucosal blood flow and cell growth [21,22], the observed effect of 16,16-dmPGE2 may in part be attributed to other factors than the modification of the luminal contents in the duodenum.…”

Section: Discussionmentioning

confidence: 99%

Healing Process of Duodenal Ulcers Induced by Indomethacin plus Histamine in Rats

Takeuchi¹,

Okada²,

Niida³

et al. 1989

Digestion

View full text Add to dashboard Cite

Healing of duodenal ulcers induced by indomethacin + histamine was investigated in rats. Animals were treated with indomethacin (5 mg/kg, s.c, once daily) and histamine (40 mg/kg, s.c, 3 times every 2.5 h after indomethacin treatment) for 2 days under fasting conditions, and they were fed normally thereafter. The duodenal ulcers so induced were confined to the proximal part of the duodenum and penetrated to the muscular mucosa with an incidence of over 80% when determined 32 h after the first injection of indomethacin (day 1). The ulcers became smaller and shallower within 7 days with granulation from the ulcer base, the mucosa grew in from the edges over the surface of granulation tissue, and they had healed almost completely after 15 days with epithelial regeneration from the edge of the ulcers. The healing of ulcers was significantly promoted by a 5-day treatment with an antacid (Al(OH)₃) as well as antisecretory agents (omeprazole, cimetidine, propantheline bromide) and 16,16-dimethyl prostaglandin E₂ at the dose which produced a potent inhibition of acid output and a marked increase in duodenal alkaline secretion. These results suggest that the duodenal ulcers induced in rats by indomethacin + histamine may provide a useful model for studying the healing process of duodenal ulcers and for the evaluation of the drugs with possible effects on ulcer healing.

show abstract

“…[10][11][12][13][14] In the dermis, COX-2 up-regulation follows the initial injury, participates in the subsequent inflammatory phase, and appears to contribute to the degree of eventual fibrosis, 15,16 primarily through one of its products, prostaglandin E2 (PGE2). [17][18][19] PGE2 in turn modulates the activity of a wide variety of cells, including keratinocytes, 20 dendritic cells, 21 and fibroblasts 22 via four E-prostanoid (EP) receptors, EP1-EP4, coupled to calcium and cAMP intracellular signaling, which belong to the larger family of G-coupled protein receptors. [23][24][25][26] The precise receptor expression profile appears to be important in determining the overall effect of PGE2, which can be either pro-or antiinflammatory, and the EP profile is differentially regulated during fetal and adult wound healing.…”

mentioning

confidence: 99%

Prostaglandin E2 differentially modulates human fetal and adult dermal fibroblast migration and contraction: implication for wound healing

Sandulache

Parekh

Li-Korotky

et al. 2006

Wound Repair Regeneration

View full text Add to dashboard Cite

Cyclooxygenase-2 is up-regulated shortly after dermal injury and it has been shown to have important activity during the repair process. Its main product in the skin, prostaglandin E2 (PGE2), modulates both inflammatory and fibrotic processes during wound healing and partially dictates the overall outcome of wound healing. PGE2 signaling has been shown to be altered during fetal wound healing. This study was designed to examine the mechanism(s) by which PGE2 regulates fibroblast migration and contraction and to determine whether these mechanisms are conserved in fetal-derived dermal fibroblasts. Fetal and adult dermal fibroblasts express all four PGE2 receptors. PGE2 inhibits fetal and adult fibroblast migration in a dose-dependent manner through the EP2/EP4-cAMP-protein kinase A pathway. However, fetal fibroblasts appear to be refractory to this effect, requiring a 10-fold higher concentration of PGE2 to achieve a similar degree of inhibition as adult fibroblasts. Inhibition of adult fibroblast migration correlated with disruption of the actin cytoskeleton. In contrast, PGE2 or a cAMP analog did not disrupt the actin cytoskeleton of fetal dermal fibroblasts. These findings were extended using a modified free-floating, fibroblast-populated collagen lattice (FPCL) contraction assay designed to measure fibroblast contraction. PGE2-inhibited FPCL contraction by adult fibroblasts, but fetal fibroblasts exhibited higher rates of FPCL contraction and a blunted response to exogenous modulation by PGE2 or a cyclase activator (forskolin). These findings indicate that fetal dermal fibroblasts are partially refractory to the effects of PGE2, a major inflammatory mediator associated with dermal wound healing. This effect may have significant and specific relevance to the scarless fetal wound-healing phenotype.

show abstract

Effect of prostaglandins on protein, RNA, DNA and collagen synthesis in experimental wounds

Cited by 45 publications

References 5 publications

Short term supplementation of dietary antioxidants selectively regulates the inflammatory responses during early cutaneous wound healing in diabetic mice

Short term supplementation of dietary antioxidants selectively regulates the inflammatory responses during early cutaneous wound healing in diabetic mice

Healing Process of Duodenal Ulcers Induced by Indomethacin plus Histamine in Rats

Prostaglandin E2 differentially modulates human fetal and adult dermal fibroblast migration and contraction: implication for wound healing

Contact Info

Product

Resources

About