Michael posterino skin#

Extracellular matrix remodeling and matrix metalloproteinases in the vascular wall during aging and in pathological conditions. Response of matrix metalloproteinases and tissue inhibitors of metalloproteinases messenger ribonucleic acids to ovarian steroids in human endometrial explants mimics their gene and phase-specific differential control in vivo. Vassilev V, Pretto CM, Coronet PB, et al. Impaired endothelial function and increased carotid stiffness in 9-year old children with low birth-weight. Sodium intake, large artery stiffness, and proteoglycans in the spontaneously hypertensive rat. Contribution of chondroitin-dermatan sulfate-containing proteoglycans to the function of rat mesenteric arteries. Gandley RE, McLaughlin MK, Koob TJ, Little SA, McGuffee LJ. Role of elastin in spontaneously hypertensive rat small mesenteric artery remodeling. Structural and genetic bases of arterial stiffness. Impaired angiogenesis in aging is associated with alterations in vessel density, matrix composition, inflammatory response, and growth factor expression. Karnik SK, Brooke BS, Bayes-Genis A, et al.A critical role for elastin signaling in vascular morphogenesis and disease. Kielty CM, Sherratt MJ, Marson A, Baldock C. Maternal food restricts (FR) induces remodeling of the vascular extracellular matrix in the offspring. Momeni M, Han G, Ross MG, Desai M, Khorram O. Programmed obesity in intrauterine growth-restricted newborns: modulation by newborn nutrition. Evidence for posttranscriptional modulation.

Michael posterino skin#

Kahari VM, Olsen DR, Rhudy RW, Carrillo P, Chen YQ, Uitto J.Transforming growth factor-beta up-regulates elastin gene expression in human skin fibroblasts. Effect of age and IGF-I administration on elastin gene expression in rat aorta. 2001 189:266–274.įoster JA, Rich CB, Miller M, Benedict MR, Richman RA, Florini JR. Proteoglycan of the extracellular matrix and growth control. Characteristics of the aortic elastic network and related phenotypes in seven inbred rat strains. Physiol Rev.1978 58:397–460.īehmoaras J, Osborne-Pellegrin M, Gauguier D, Jacob MP. Mechanisms underlying the programming of small artery dysfunction: review of the model using low protein diet in pregnancy in the rat. Developmental programming of aortic and renal structure in offspring of rats fed fat-rich diets in pregnancy. Microvascular rarefaction and decreased angiogenesis in rats with fetal programming of hypertension associated with exposure to a low protein diet in utero. Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. Low birth weight and risk of high blood pressure in adulthood. Death rates from stroke in England and Wales predicted from past maternal mortality. By 2 months of life, the compositions of both vessel types are consistent with stiff vessels, a contributing factor to hypertension.īarker DJ, Osmond C. These results indicate a significant remodeling of the extracellular matrix occurs in both conduit and resistance vessels. There was a significant increase in expression of matrix metalloproteinase 9 (MMP-9) mRNA in 1-day-old MFR aortas, while both MMP-9 and MMP-2 expression was increased in the 4-month-old MFR aortas. There were no changes in elastin in both age groups in mesenteric arterioles, and by 2 months of life, collagen deposition was also found in these resistance vessels. In mesenteric arterioles of MFR offspring, there was a decrease in GAG in 1-day-old and 2-month-old MFR offspring.

A redistribution of elastin was also noted in MFR offspring, with a significant decrease in the interelastin laminae at both 1 day and 2 months. By 2 months of life, there was a significant increase in collagen and a decrease in GAG in MFR offspring aortas. In aortas of MFR offspring, there was a significant increase in elastin and glycosaminoglycans (GAG) at 1 day of age. To test this hypothesis, the authors studied the blood vessels of offspring of dams that were exposed to 50% maternal food restriction (MFR) from e10 to term as compared to age-matched controls. The authors hypothesized that maternal nutritional restriction prenatally induces remodeling of offspring blood vessels such that they become stiff and contribute to the development of adult hypertension. The uterine environment may influence the development of chronic diseases later in life.