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Kapur, A.

Publications and source records attributed to Kapur, A..

3 recordsLinked to original sources

Murine implantation chamber formation precedes natural and artificial decidualization

During pregnancy uterine stromal cells undergo a mesenchymal to epithelial cell transition termed decidualization. In humans initiation of decidualization occurs in the absence of an embryo resulting in a need to identify embryo-independent molecular cues that can initiate decidualization. Although, similar to humans, decidualization in the mouse can be induced in the absence of an embryo, whether an implantation event is prerequisite for such decidualization is not known. In this study using different models of estrogen-dependent implantation, including natural (embryo) and artificial (sesame oil, agarose only beads, and Concanavalin A coated agarose beads) we determined that implantation chamber formation precedes decidualization. We show that focal stimuli, including the embryo, Concanavalin A coated bead, and oil droplets, induce V-shaped implantation chambers that lead to sub-epithelial PTGS2 expression and decidualization. Unfertilized eggs and uncoated agarose blue beads fail to form an implantation chamber and do not initiate decidualization. Further, we show that lectins that share sugar binding properties with Concanavalin A can also induce a V-shaped implantation chamber. Finally, using second harmonic generation we show that during decidualization collagen fibers spread radially away from the implantation chamber irrespective of the focal signal used for inducing the chamber. Thus, in the mouse artificial decidualization also initiates at the site of implantation chamber formation. These findings are critical when separating physical stimulus-dependent, embryo-dependent and embryo-independent mechanisms of decidualization that underlie a successful pregnancy.

developmental biology↗

FGF21 Normalizes Plasma Glucose in Mouse Models of Type 1 Diabetes and Insulin Receptor Dysfunction

Fibroblast growth factor 21 (FGF21) is a member of the fibroblast growth factor (FGF) family of proteins. The biological activity of FGF21 was first shown to induce insulin independent glucose uptake in adipocytes through the GLUT1 transporter. Subsequently, it was shown to have effects on the liver to increase fatty acid oxidation. FGF21 treatment provides beneficial metabolic effects in both animal models and patients with obesity, type 2 diabetes mellitus (T2D) and/or fatty liver disease. In this paper, we revisited the original finding and found that insulin independent glucose uptake in adipocytes is preserved in the presence of an insulin receptor antagonist. Using a 40 kDa PEGylated (PEG) and half-life extended form of FGF21 (FGF21-PEG), we extended these in vitro results to two different mouse models of diabetes. FGF21-PEG normalized plasma glucose in streptozotocin-treated mice, a model of type 1 diabetes (T1D), without restoring pancreatic {beta}-cell function. FGF21-PEG also normalized plasma glucose levels and improved glucose tolerance in mice chronically treated with an insulin competitive insulin receptor antagonist, a model of autoimmune/Type-B insulin resistance. These data extend the pharmacological potential of FGF21 beyond the settings of T2D, fatty liver and obesity.

pharmacology and toxicology↗

Plumbagin-induced oxidative stress leads to inhibition of Na+/K+-ATPase (NKA) in canine cancer cells.

The Na+/K+-ATPase (NKA) complex is the master regulator of membrane potential and a target for anti-cancer therapies. Here, we investigate the effect of drug-induced oxidative stress on NKA activity. The natural product, plumbagin increases oxygen radicals through inhibition of oxidative phosphorylation. As a result, plumbagin treatment results in decreased production of ATP and a rapid increase in intracellular oxygen radicals. We show that plumbagin induces apoptosis in canine cancer cells via oxidative stress. We use this model to test the effect of oxidative stress on NKA activity. Using whole-cell patch-clamp electrophysiology we demonstrate that short-term exposure (4 min) to plumbagin results in 48% decrease in outward current at +50 mV. Even when exogenous ATP was supplied to the cells, plumbagin treatment resulted in 46% inhibition outward current through NKA at +50 mV. In contrast, when the canine cancer cells were pre-treated with the oxygen radical scavenger, N-acetylcysteine, the NKA inhibitory activity of plumbagin was abrogated. These experiments demonstrate that the oxidative stress-causing agents such as plumbagin and its analogues, are a novel avenue to regulate NKA activity in tumors.

cancer biology↗