Active matrix metalloproteinase‐2 upregulation in the abdominal skin of patients with direct inguinal hernia

Pascual, Gemma; Rodríguez, Marta; Gómez-Gil, Verónica; Trejo, Cynthia; Buján, Julia

doi:10.1111/j.1365-2362.2010.02364.x

Cited by 30 publications

(24 citation statements)

References 29 publications

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“…Also, MMP activity could be influenced by other MMP activators and inhibitors. In effect, some MMPs may cleave other pro-MMPs, and membrane-type 1-MMP is a key activator of pro-MMP-2 [37, 92, 94]. Also, tissue inhibitors of metalloproteinases (TIMPs) are endogenous modulators of MMPs [92, 94, 95], and the regional changes in uteroplacental TIMPs in HTN-Preg need to be examined.…”

Section: Discussionmentioning

confidence: 99%

Angiogenic imbalance and diminished matrix metalloproteinase-2 and -9 underlie regional decreases in uteroplacental vascularization and feto-placental growth in hypertensive pregnancy

Dias‐Junior

Chen

Cui

et al. 2017

Biochemical Pharmacology

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Preeclampsia is a form of hypertension-in-pregnancy (HTN-Preg) with unclear mechanism. Generalized reduction of uterine perfusion pressure (RUPP) could be an initiating event leading to uteroplacental ischemia, angiogenic imbalance, and HTN-Preg. Additional regional differences in uteroplacental blood flow could further affect the pregnancy outcome and increase the risk of preeclampsia in twin or multiple pregnancy, but the mechanisms involved are unclear. To test the hypothesis that regional differences in angiogenic balance and matrix metalloproteinases (MMPs) underlie regional uteroplacental vascularization and feto-placental development, we compared fetal and placental growth, and placental and myoendometrial vascularization in the proximal, middle and distal regions of the uterus (in relation to the iliac bifurcation) in normal pregnant (Preg) and RUPP rats. Maternal blood pressure and plasma anti-angiogenic soluble fms-like tyrosine kinase-1 (sFlt-1)/placenta growth factor (PIGF) ratio were higher, and average placentae number, placenta weight, litter size, and pup weight were less in RUPP than Preg rats. The placenta and pup number and weight were reduced, while the number and diameter of placental and adjacent myoendometrial arteries, and MMP-2 and MMP-9 levels/activity were increased, and sFlt-1/PlGF ratio was decreased in distal vs proximal uterus of Preg rats. In RUPP rats, the placenta and pup number and weight, the number and diameter of placental and myoendometrial arteries, and MMP-2 and -9 levels/activity were decreased, and sFlt-1/PlGF ratio was increased in distal vs proximal uterus. Treatment with sFlt-1 or RUPP placenta extract decreased MMP-2 and MMP-9 in distal segments of Preg uterus, and treatment with PIGF or Preg placenta extract restored MMP levels in distal segments of RUPP uterus. Thus, in addition to the general reduction in placental and fetal growth during uteroplacental ischemia, localized angiogenic imbalance and diminished MMP-2 and MMP-9 could cause further decrease in placental and myoendometrial vascularization and placental and fetal growth in distal vs proximal uterus of HTN-Preg rats. Regional differences in uteroplacental perfusion, angiogenic balance and MMPs could be a factor in the incidence of preeclampsia in multiple pregnancy.

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Section: Discussionmentioning

confidence: 99%

Angiogenic imbalance and diminished matrix metalloproteinase-2 and -9 underlie regional decreases in uteroplacental vascularization and feto-placental growth in hypertensive pregnancy

Dias‐Junior

Chen

Cui

et al. 2017

Biochemical Pharmacology

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“…For example, some MMPs may cleave other pro-MMPs, and membrane-type (MT)1-MMP is a key activator of pro-MMP-2 [14, 15, 38, 67]. On the other hand, tissue inhibitors of MMPs (TIMP-1 and TIMP-2) are endogenous modulators of MMPs activity [14, 15, 38, 67], and the changes in their expression/activity in HTN-Preg need to be examined. Also, in the present study the changes in uterine, placental and aortic MMPs were measured at day 19 of gestation, and the progressive changes during the course of pregnancy and their reversal in the postpartum period need to be examined.…”

Section: Discussionmentioning

confidence: 99%

Altered matrix metalloproteinase-2 and -9 expression/activity links placental ischemia and anti-angiogenic sFlt-1 to uteroplacental and vascular remodeling and collagen deposition in hypertensive pregnancy

Mata

Mazzuca

et al. 2014

Biochemical Pharmacology

100

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Preeclampsia is a complication of pregnancy manifested as maternal hypertension and often fetal growth restriction. Placental ischemia could be an initiating event, but the linking mechanisms leading to hypertension and growth restriction are unclear. We have shown an upregulation of matrix metalloproteinases (MMPs) during normal pregnancy (Norm-Preg). To test the role of MMPs in hypertensive-pregnancy (HTN-Preg), maternal and fetal parameters, MMPs expression, activity and distribution, and collagen and elastin content were measured in uterus, placenta and aorta of Norm-Preg rats and in rat model of reduced uteroplacental perfusion pressure (RUPP). Maternal blood pressure was higher, and uterine, placental and aortic weight, and the litter size and pup weight were less in RUPP than Norm-Preg rats. Western blots and gelatin zymography revealed decreases in amount and gelatinase activity of MMP-2 and MMP-9 in uterus, placenta and aorta of RUPP compared with Norm-Preg rats. Immunohistochemistry confirmed reduced MMPs in uterus, placenta and aortic media of RUPP rats. Collagen, but not elastin, was more abundant in uterus, placenta and aorta of RUPP than Norm-Preg rats. The anti-angiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1) decreased MMPs in uterus, placenta and aorta of Norm-Preg rats, and vascular endothelial growth factor (VEGF) reversed the decreases in MMPs in tissues of RUPP rats. Thus placental ischemia and anti-angiogenic sFlt-1 decrease uterine, placental and vascular MMP-2 and MMP-9, leading to increased uteroplacental and vascular collagen, and growth-restrictive remodeling in HTN-Preg. Angiogenic factors and MMP activators may reverse the decrease in MMPs and enhance growth-permissive remodeling in preeclampsia.

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“…The degrading limb of the dynamic homeostatic process of collagen metabolism has been evaluated by measuring the levels of MMPs in abdominal wall fascial 48 Several studies have demonstrated an MMP-2 overexpression in both transversalis fascia and skin fibroblasts from patients with direct inguinal hernias compared with controls. 43,49,50 Research conducted in our institution demonstrated an imbalance of MMP/TIMP activity at both the local tissue level and systemic circulation, indicating a dysregulation of the extracellular matrix degradation process. 51 Furthermore, several authors have shown an association between MMP-1 and MMP-13 activity and recurrent inguinal and incisional hernia, suggesting a disturbed process of wound healing as their underlying etiology (Table).…”

Section: Mechanisms Of Connective Tissue Metabolism For Aneurysm and mentioning

confidence: 99%

Abdominal aortic aneurysm and abdominal wall hernia as manifestations of a connective tissue disorder

Antoniou

Georgiadis

Antoniou

et al. 2011

Journal of Vascular Surgery

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Active matrix metalloproteinase‐2 upregulation in the abdominal skin of patients with direct inguinal hernia

Cited by 30 publications

References 29 publications

Angiogenic imbalance and diminished matrix metalloproteinase-2 and -9 underlie regional decreases in uteroplacental vascularization and feto-placental growth in hypertensive pregnancy

Angiogenic imbalance and diminished matrix metalloproteinase-2 and -9 underlie regional decreases in uteroplacental vascularization and feto-placental growth in hypertensive pregnancy

Altered matrix metalloproteinase-2 and -9 expression/activity links placental ischemia and anti-angiogenic sFlt-1 to uteroplacental and vascular remodeling and collagen deposition in hypertensive pregnancy

Abdominal aortic aneurysm and abdominal wall hernia as manifestations of a connective tissue disorder

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