It is well known that cardiovascular disease is less frequent in premenopausal women compared with men but rises rapidly in postmenopausal women. Such early observations led to the hypothesis that estrogen therapy will reduce the risk of postmenopausal women developing cardiovascular disease.(1) However, observational studies have led to conflicting results with some studies reporting reductions in cardiovascular disease in postmenopausal women taking estrogens whilst others observed no beneficial effects.(2) Rather increases in the risk of coronary heart disease and stroke have been reported, particularly for women who are older and those with a long hormone-free interval.(3) Such findings have led to the speculation that estrogens have competing cardiovascular effects-beneficial and detrimental and this has intensified efforts to better understand the range of cardiovascular effects mediated by estrogens and their signaling mechanisms, the ultimate aim being to develop new therapies for women that exert the beneficial effects of estrogen whilst minimizing potentially harmful effects. To achieve this aim, new studies to better understand both nuclear and membrane estrogen receptor (ER)-mediated signaling in target tissues such as the heart and blood vessels, immune cells and other target tissues are in progress. In this issue of Circulation, Moens and colleagues provide novel insights on the importance of membrane ER-mediated signaling pathways in blood vessels for vasoprotection and vascular gene regulation.(4).
"In males, the ACE/AngII/AGTR1 pathways are enhanced, whereas, in females, the balance is shifted towards the ACE2/Ang(1-7)/MasR (Mas receptor) and angiotensin type 2 receptor (AT2R) pathways . Studies reported that premenopausal women, as compared to age matched men, are protected from renal and cardiovascular disease, and this differential balance of the RAS between the sexes likely contributes [80, 81]. "
[Show abstract][Hide abstract] ABSTRACT: Renin-angiotensin system (RAS) polymorphisms have been studied as candidate risk factors for hypertension with inconsistent results, possibly due to heterogeneity among various genetic and environmental factors. A case-control association study was conducted to investigate a possible involvement of polymorphisms of three RAS genes:AGT M235T (rs699),ACEI/D (rs4340) and G2350A (rs4343), andAGTR1A1166C (rs5186) in essential hypertensive patients. A total of 211 cases and 211 controls were recruited for this study. Genotyping was performed using PCR-RFLP method. The genotype and allele distribution of the M235T variant differed significantly in hypertensives and normotensives (OR-CI = 2.62 (1.24–5.76), 𝑃 = 0.006; OR-CI = 0.699 (0.518–0.943),𝑃 = 0.018), respectively. When the samples were segregated based on sex, the 235TT genotype and T allele were predominant
in the female patients (OR-CI = 5.68 (1.60-25.10), 𝑃 = 0.002; OR-CI = 0.522 (0.330–0.826), 𝑃 = 0.005) as compare to the male patients (OR-CI = 1.54 (1.24–5.76), 𝑃 = 0.34; OR-CI = 0.874 (0.330–0.826), 𝑃 = 0.506), respectively. For ACE DD variant, we found overrepresentation of “I”-allele (homozygous II and heterozygous ID) in unaffected males which suggest its protective role in studied population (OR-CI = 0.401 (0.224–0.718); 𝑃 = 0.0009). The M235T variant of the AGT is significantly associated with female hypertensives andACE DD variant could be a risk allele for essential hypertension in south India.
[Show abstract][Hide abstract] ABSTRACT: Proteins of the striatin family (striatins 1-4; sizes ranging from 90 to 110 kDa on SDS-polyacrylamide gel electrophoresis) are highly homologous in their amino acid sequences but can differ in their cell-type-specific gene expression patterns and biological functions. In various cell types, we have found one, two or three polypeptides of this evolutionarily old and nearly ubiquitous family of proteins known to serve as scaffold proteins for diverse protein complexes. Light and electron microscopic immunolocalization methods have revealed striatins in mammalian cell-cell adherens junctions (AJs). In simple epithelia, we have localized striatins as constitutive components of the plaques of the subapical zonulae adhaerentes of cells, including intestinal, glandular, ductal and urothelial cells and hepatocytes. Striatins colocalize with E-cadherin or E-N-cadherin heterodimers and with the plaque proteins α- and β-catenin, p120 and p0071. In some epithelia and carcinomas and in cultured cells derived therefrom, striatins are also seen in lateral AJs. In stratified epithelia and in corresponding squamous cell carcinomas, striatins can be found in plaques of some forms of tessellate junctions. Moreover, striatins are major plaque proteins of composite junctions (CJs; areae compositae) in the intercalated disks connecting cardiomyocytes, colocalizing with other CJ molecules, including plectin and ankyrin-G. We discuss the “multimodulator” scaffold roles of striatins in the initiation and regulation of the formation of various complex particles and structures. We propose that striatins are included in the diagnostic candidate list of proteins that, in the CJs of human hearts, can occur in mutated forms in the pathogeneses of hereditary cardiomyopathies, as seen in some types of genetically determined heart damage in boxer dogs.
Cell and Tissue Research 12/2014; 359(3):779-797. DOI:10.1007/s00441-014-2053-z · 3.57 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.