Anti-Human APLN Polyclonal antibody

Suboptimal conditions in pregnancy can elicit long-term effects on the health of offspring. The most common outcome is programmed hypertension. We examined whether there are common genes and pathways in the kidney are responsible for generating programmed hypertension among three different models using next generation RNA sequencing (RNA-Seq) technology. Pregnant Sprague-Dawley rats received dexamethasone (DEX, 0.1 mg/kg) from gestational day 16 to 22, 60% high-fructose (HF) diet, or N-G-nitro-l-arginine-methyester (l-NAME, 60 mg/kg/day) to conduct DEX, HF, or l-NAME model respectively. All three models elicited programmed hypertension in adult male offspring. We observed five shared genes (Bcl6, Dmrtc1c, Egr1, Inmt, and Olr1668) among three different models. The identified differential genes (DEGs) that are related to regulation of blood pressure included Aqp2, Ptgs1, Eph2x, Hba-a2, Apln, Guca2b, Hmox1, and Npy. RNA-Seq identified genes in arachidonic acid metabolism are potentially gatekeeper genes contributing to programmed hypertension. In addition, HF and DEX increased expression and activity of soluble epoxide hydrolase (Ephx2 gene encoding protein). Conclusively, the DEGs in arachidonic acid metabolism are potentially gatekeeper genes in programmed hypertension. The roles of DEGs identified by the RNA-Seq in this study deserve further clarification, to develop the potential interventions in the prevention of programmed hypertension.

Background. Nephropathy associated with antiphospholipid antibodies (aPL) has been proposed as a risk factor of worse renal prognosis in patients with systemic lupus erythematosus (SLE). The purpose of the current study was to evaluate the prevalence of aPL-associated nephropathy (aPLN) among patients with lupus nephritis and to describe their functional renal outcome. Methods. A total of 79 renal biopsies from 77 patients followed at the Hospital Clinic, Spain were analysed. Each renal biopsy was evaluated by a pathologist who was blinded to the aPL status. Thrombotic microangiopathy (TMA), fibrous intimal hyperplasia (FIH), fibrocellular arterial occlusion (FAO), focal cortical atrophy (FCA), and tubular thyroidization as lesions suggestive of aPLN were identified. Results: aPLN was found in nine (11.4%) biopsies. TMA was found in three (33.3%) cases whereas chronic aPLN, represented by FIH and FCA, was found in four (44.4%) and three (33.3%) cases, respectively. A significant association between the presence of aPL and aPLN was found (p = 0.003). Patients with lupus anticoagulant (LA) plus IgG anticardiolipin antibodies (aCL) showed an increased prevalence of aPLN (OR: 3.61, 95% CI 1.28-5.14; p = 0.002). Creatinine levels were significantly increased in patients with aPLN compared with those with aPL without aPLN (p = 0.038). However, no significant difference in complete remission, partial remission, not response, and established renal damage between groups was observed at the end of follow-up. Conclusions: The aPL have an important role in the pathogenesis of renal lesions in SLE patients. Prospective studies are needed to address the role of aPLN in the long-term outcome of SLE patients with positive aPL. Lupus (2011) 20, 721-729.