Regulation of matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1 by dichloroacetic acid in human fibroblasts from normal peritoneum and adhesions

Diamond, Michael P.; El-Hammady, Eslam; Wang, Rona; Saed, Ghassan M.

doi:10.1016/j.fertnstert.2003.05.006

Cited by 23 publications

(26 citation statements)

References 19 publications

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“…However, in several pathological cases, including fibrosis, myofibroblastic differentiation persists and causes excessive scarring [24,25]. In fact, postoperative adhesions, like fibrosis, reflect a pathologic excess of biologic events involved in normal tissue repair, and myofibroblasts can be considered responsible for postoperative adhesions as they are the primary source of the increased extracellular matrix protein expression, as well as a major source of fibrogenic growth factors, such as TGF-β1 [26][27][28][29][30]. This cytokine controls crucial cellular end points, including cell proliferation, differentiation, apoptosis, tissue morphogenesis, and wound healing [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-generated superoxide induces the development of the adhesion phenotype

Fletcher

Jiang

Diamond

et al. 2008

Free Radical Biology and Medicine

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Adhesion fibroblasts exhibit higher TGF-β1 and type I collagen expression as compared to normal peritoneal broblasts. Furthermore, exposure of normal peritoneal fibroblasts to hypoxia results in an irreversible increase in TGF-β1 and type I collagen. We postulated that the mechanism by which hypoxia induced the adhesion phenotype is through the production of superoxide either directly or through the formation of peroxynitrite. To test this hypothesis, normal peritoneal and adhesion fibroblasts were treated with superoxide dismutase (SOD), a superoxide scavenger, and xanthine/ xanthine oxidase, a superoxide-generating system, under normoxic and hypoxic conditions. Also, cells were treated with peroxynitrite. TGF-β1 and type I collagen expression was determined before and after all treatments using real-time RT/PCR. Hypoxia treatment resulted in a time-dependent increase in TGF-β1 and type I collagen mRNA levels in both normal peritoneal and adhesion fibroblasts. Similarly, treatment with xanthine oxidase, to endogenously generate superoxide, resulted in higher mRNA levels of TGF-β1 and type I collagen in both normal peritoneal and adhesion fibroblasts. In contrast, treatment with SOD, to scavenge endogenous superoxide, resulted in a decrease in TGF-β1 and type I collagen expression in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts; no effect on the expression of these molecules was seen in normal peritoneal fibroblasts. Exposure to hypoxia in the presence of SOD had no effect on mRNA levels of TGF-β1 and type I collagen in either normal peritoneal or adhesion fibroblasts. Peroxynitrite treatment alone significantly induced both adhesion phenotype markers. In conclusion, hypoxia, through the production of superoxide, causes normal peritoneal fibroblasts to acquire the adhesion phenotype. Scavenging superoxide, even in the presence of hypoxia, prevented the development of the adhesion phenotype. These findings further support the central role of free radicals in the development of adhesions.

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Section: Discussionmentioning

confidence: 99%

Hypoxia-generated superoxide induces the development of the adhesion phenotype

Fletcher

Jiang

Diamond

et al. 2008

Free Radical Biology and Medicine

Self Cite

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“…It was also confirmed by the absence of pneumoperitoneum-enhanced adhesions in mice deficient for the genes encoding for factors regulated by hypoxia such as HIFs [54], VEGF [30] and PAI-1 [29]. The important role of hypoxia in adhesion formation was further supported by a series of in vitro studies demonstrating increased expression of many adhesiogenic factors produced by fibroblasts cultured under hypoxic conditions [62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77][78][79].…”

Section: Discussionmentioning

confidence: 93%

Angiogenic factors in peritoneal adhesion formation

Molinas¹,

Binda

Koninckx

2006

Gynecol Surg

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Abdominal surgery is considered as the leading cause of peritoneal adhesions and almost universally as adhesiogenic. Peritoneal injury at the time of surgery initiates an inflammatory reaction determining fibrin deposition on the wound surface. Depending on the balance between the different components of the plasminogen system, this fibrin can be either lysed, leading to normal peritoneal healing, or organised, serving as a scaffold for fibroblast ingrowth, extracellular matrix deposition and angiogenesis, leading to adhesion formation. The mechanism underlying the predisposition to form adhesions in some patients and in some specific anatomic sites and not in others after similar surgical procedures remains unknown. In spite of the many attempts proposed over the years for reducing the incidence of adhesion formation, peritoneal adhesions remain a major clinical problem, inducing intestinal obstruction, pelvic pain, female infertility and difficulties at the time of re-operation. The available evidence indicates that understanding the adhesion formation process at the molecular level is essential for developing successful strategies for preventing adhesions. Fortunately, the advancement in molecular biology during the last years has led to the identification of many molecules with the potential of regulating inflammatory and immune responses, tissue remodelling and angiogenesis, key events in peritoneal healing and adhesion formation. This review focuses on the role of angiogenesis and angiogenic factors in peritoneal adhesion formation.

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“…Фибробласты и макрофаги форми-руют коллаген, образуется матрикс и освобождаются продукты деградации фибрина (FDPs). Но, если ма-трикс прикрепился к брюшине, образуется фибрин [11]. В перитонеальной жидкости также повышается активность провоспалительных цитокинов фактора некроза опухоли-α, интерлейкина-6 и снижается экспрессия их ингибиторов (интерлейкина-10, интерферона-γ) при наличии спаек.…”

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The risk of postoperative adhesions in gynecology and their prevention

Тихомиров¹,

Gevorkyan²,

Sarsaniya³

2016

Probl. reprod.

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В связи с увеличением общего количества хирур-гических вмешательств в акушерстве и гинекологии, широким распространением повторных лапароско-пических операций (диагностические, малоинва-зивные вмешательства на яичниках и маточных тру-бах, повторные лапароскопические вмешательства по поводу эндометриоза, лапароскопические миом-эктомии и др.) в последнее время наблюдается тен-денция к увеличению числа пациенток со спайками в малом тазу и полости матки. В гинекологии тазо-вые перитонеальные спайки после операций диагно-стируют у 15-80% пациенток. Самым частым ме-стом локализации спаек являются яичники и маточ-ные трубы: одно-или двусторонняя окклюзия ма-точных труб вследствие спаечного процесса форми-руется у 15% пациенток после обычной аппендэкто-мии, окклюзия маточных труб вследствие спаечного процесса развивается у 60-80% пациенток после оперативных вмешательств на яичниках, по поводу трубной беременности, особенно выполненных по экстренным показаниям [1,2].Резидуальными осложнениями спаечного про-цесса малого таза являются: абдоминальный/тазо- Прогноз в отношении репродуктивной функции и качества дальнейшей жизни при гинекологических операциях во многом определяется возможным спаечным процессом. Адекватная интраоперационная антиадгезивная профилактика в гинекологии с использованием комплексного геля, содержащего в своем составе гиалуроновую кислоту и карбоксиметилцеллюлозу, способствует снижению риска образования спаек в малом тазу и их резидуальных осложнений. Forecast with respect to of reproductive function and quality of further life after gynecological operations is mainly determined by possible postoperative adhesions. Adequate intra-operating antiadhesivе prevention with the use of a complex gel which contains hyaluronic acid and carboxymethylcellulose contributes to reduction the risk of the pelvic adhesions and adhesion-related complications.

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Regulation of matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1 by dichloroacetic acid in human fibroblasts from normal peritoneum and adhesions

Cited by 23 publications

References 19 publications

Hypoxia-generated superoxide induces the development of the adhesion phenotype

Hypoxia-generated superoxide induces the development of the adhesion phenotype

Angiogenic factors in peritoneal adhesion formation

The risk of postoperative adhesions in gynecology and their prevention

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