Publications by authors named "Animesh Chowdhury"
CD95L (also known as FasL or CD178) is a member of the tumor necrosis family (TNF) superfamily. Although this transmembrane ligand has been mainly considered as a potent apoptotic inducer in CD95 (Fas)-expressing cells, more recent studies pointed out its role in the implementation of non-apoptotic signals. Accordingly, this ligand has been associated with the aggravation of inflammation in different auto-immune disorders and in the metastatic occurrence in different cancers.
View Article and Find Full Text PDFIn this paper we propose a new family of algorithms, ATENT, for training adversarially robust deep neural networks. We formulate a new loss function that is equipped with an additional entropic regularization. Our loss function considers the contribution of adversarial samples that are drawn from a specially designed distribution in the data space that assigns high probability to points with high loss and in the immediate neighborhood of training samples.
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- * AngII activates certain proteins like PKC-ζ, NADPH oxidase, and PKC-α, which leads to decreased AC activity and cAMP production, and this effect can be reversed by pertussis toxin.
- * The study reveals a signaling pathway involving PKC-ζ, NADPH oxidase, and PKC-α that is essential for AngII's action on inhibiting AC activity via phosphorylation of Giα2 proteins.
A recent experiment has revealed that additive free ester hydrogenation by Co-pincer complexes might follow an unusual non-bifunctional mechanism, however, the detailed mechanistic pathway is missing. It has been predicted that several intermediates and transition states are involved, having their essential role in the catalytic performances. Detailed theoretical studies are therefore essential in this regard for achieving more efficient ester hydrogenation catalysts.
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- The study investigates how a specific signaling pathway involving MMP-2 and sphingosine-1-phosphate (S1P) affects the proliferation of pulmonary artery smooth muscle cells (PASMCs) when stimulated by endothelin-1 (ET-1).
- Results show that ET-1 significantly increases NADPH oxidase and MMP-2 activities, as well as other signaling components that lead to enhanced cell proliferation.
- The tea catechin epigallocatechin-3-gallate (EGCG) is found to inhibit these effects of ET-1 by blocking the activation of NADPH oxidase and reducing the associated signaling activity, suggesting a protective role for EGCG in preventing PASMC proliferation.
Hydride transfer is the most crucial step for the catalytic hydrogenation of CO in homogeneous condition. Here, we perform state-of-the-art calculations to show the effect of geometry and spin states of Ni-hydride complexes containing different types of multidentate phosphine ligands on their hydride transfer barrier. For doing this, we first choose Ni-bis(diphosphine) complexes of the type NiP, which have been synthesized recently and then by extrapolating the idea we propose a new type of NiPN complex showing much lower hydride transfer barrier.
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- - The study examines how growth factors (GFs) and glucocorticoids (GCs) interact during cell development and disease, revealing that transcription factors like p53 and NF-κB are involved in this crosstalk.
- - GCs inhibit GFs' positive feedback while promoting inhibitory loops, and this interaction does not affect DNA methylation but can broaden the range of genes activated by GFs when demethylation occurs.
- - GFs enhance the GC receptor's binding to DNA to support gene activation, whereas GCs and GFs have opposing effects on chromatin modifications, highlighting complex regulatory mechanisms in gene expression.
Article Synopsis
- Treatment with the thromboxane A2 receptor antagonist SQ29548 effectively inhibited the activities of phospholipase D (PLD) and NADPH oxidase in human pulmonary artery smooth muscle cells (HPASMCs) when stimulated by U46619.
- Inhibition of PLD2, rather than PLD1, significantly reduced U46619-induced NADPH oxidase activity, highlighting the importance of PLD2 in this signaling pathway.
- The study identified a critical BFA-insensitive signaling axis involving Arf-6 and cytohesin-1, which is crucial for the activation of PLD and the subsequent stimulation of NADPH oxidase activity in response to U46619.
Article Synopsis
- Matrix metalloproteinases (MMPs) are important in lung diseases like pulmonary arterial hypertension (PAH), and green tea catechins, particularly EGCG and ECG, can help reduce MMP activities.
- A study found that EGCG and ECG inhibit both proMMP-2 and MMP-2 activities in lung cells, with strong interactions observed through computational analysis, specifically due to a component called the galloyl group.
- Additionally, the research showed that these catechins are better inhibitors of proMMP-2 compared to MMP-2, with similar strong interactions noted between catechins and another enzyme, MT1-MMP, which activates proMMP-2.
Article Synopsis
- Green tea polyphenolic catechins, particularly EGCG and ECG, have been found to prevent diseases like pulmonary hypertension, cancer, and various cardiac and neurological disorders.
- The study highlights that these catechins inhibit the activities of matrix metalloproteinase-9 (MMP-9) in cultured pulmonary artery smooth muscle cells.
- Computational analysis indicates a strong interaction between MMP-9 and EGCG/ECG, with the galloyl group of the catechins playing a crucial role in their effectiveness.
Article Synopsis
- The study investigates how angiotensin II (ANG II) stimulates the growth of pulmonary artery smooth muscle cells (PASMCs), finding that 100 nM of ANG II maximizes cell proliferation.
- It was determined that blocking the AT1 receptor and using specific inhibitors for sphingomyelinase and sphingosine kinase can prevent this cell growth triggered by ANG II.
- Additionally, the study highlights that ANG II activates various signaling pathways, including proMMP-2 expression and ERK1/2 phosphorylation, which are crucial for PASMC proliferation through the involvement of the sphingolipid signaling axis.
Article Synopsis
- Treatment with endothelin-1 (ET-1) increases the expression and activation of proMMP-2 in bovine pulmonary artery smooth muscle cells through several signaling mechanisms.
- Inhibitors targeting NADPH oxidase, PKC-α, p(38)MAPK, and NF-κB successfully block this activation and the increase in related proteins like MT1-MMP.
- The study highlights that ET-1 also reduces TIMP-2 levels, indicating potential cross-talk between various signaling pathways that regulate proMMP-2 activity.
Article Synopsis
- Tea is a globally popular beverage that contains polyphenols, which are linked to a lower risk of chronic diseases like cancer and heart issues.
- The primary polyphenol in tea, epigallocatechin-3-gallate (EGCG), is highlighted for its protective effects against these diseases, though it works mainly by interacting with cellular signaling pathways rather than direct antioxidant action.
- The review summarizes various studies, including epidemiological data and human trials, to illustrate EGCG's role in disease prevention and its underlying molecular mechanisms.
Article Synopsis
- The study focuses on how the compound epigallocatechin-3-gallate (EGCG) inhibits the growth of pulmonary artery smooth muscle cells (PASMCs) that contribute to pulmonary hypertension when induced by the thromboxane A2 mimetic U46619.
- U46619 triggers maximum cell proliferation by activating pathways including p(38)MAPK, NF-κB, and MMP-2, while also increasing the levels of sphingosine 1 phosphate (S1P) through the activation of sphingomyelinase and sphingosine kinase.
- EGCG effectively reduces U46619-induced cell proliferation by blocking these signaling pathways and preventing the activation of MMP
Article Synopsis
- Aneurysms develop from chronic inflammation damaging the structure of blood vessel proteins like elastin and collagen due to the action of inflammatory cytokines and proteases, particularly matrix metalloproteinases (MMPs).
- The plasminogen and MMPs systems, influenced by various genetic factors, play crucial roles in aneurysm development, with recent findings indicating a link between overexpression of the MMP-2 gene and aneurysm formation.
- Inhibiting MMP-2 and JNK (c-Jun N-terminal kinase) has shown promise as a therapeutic approach to slowing the progression of vascular aneurysms.
Endothelin-1 (ET-1) is known as the most potent vasoconstrictor yet described. Infusion of ET-1 into isolated rabbit lung has been shown to cause pulmonary vasoconstriction with the involvement of arachidonic acid metabolites. Given the potency of arachidonic acid metabolites, the activity of phospholipase A2 must be tightly regulated.
View Article and Find Full Text PDFTreatment of bovine pulmonary artery smooth muscle cells (BPASMCs) with U46619 attenuated isoproterenol caused stimulation of adenyl cyclase activity and cAMP production. Pretreatment with SQ29548 (Tp receptor antagonist), apocynin (NADPH oxidase inhibitor) and Go6976 (PKC-α inhibitor) eliminated U46619 caused attenuation of isoproterenol stimulated adenyl cyclase activity. Pretreatment with SQ29548 and apocynin prevented U46619 induced increase in NADPH oxidase activity, PKC-α activity and Giα phosphorylation.
View Article and Find Full Text PDFWe investigated the mechanism by which TxA2 mimetic, U46619, activates proMMP-2 in bovine pulmonary artery smooth muscle cells. Our study showed that treatment of the cells with U46619 caused an increase in the expression and subsequently activation of proMMP-2 in the cells. Pretreatment with p(38)MAPK inhibitor, SB203580; and NF-κB inhibitor, Bay11-7082 inhibited the expression and activation of proMMP-2 induced by U46619.
View Article and Find Full Text PDFWe sought to evaluate the mechanism(s) associated with pro matrix metalloprotease 2 (proMMP-2) activation in bovine pulmonary artery smooth muscle cells. Preincubation of cells with anti-TNFR1 antibody prevented tumour necrosis factor-α (TNF-α)-induced proMMP-2 activation and increase in membrane type 1 matrix metalloprotease (MT1-MMP) expression as well as inhibition of tissue inhibitor of metalloproteinase 2 (TIMP-2) expression, indicating the role of TNFR1 receptor during TNF-α stimulation. Anti-MT1-MMP antibody abrogated proMMP-2 activation by TNF-α-stimulated cell membrane, suggesting the involvement of MT1-MMP in proMMP-2 activation.
View Article and Find Full Text PDFIn the context of cross-talk between transmembrane signaling pathways, we studied the loci within the β-adrenergic receptor/G protein/adenyl cyclase system at which PKC exerts regulatory effects of peroxynitrite (ONOO(-)) on isoproterenol stimulated adenyl cyclase activity in pulmonary artery smooth muscle cells. Treatment of the cells with ONOO(-) stimulated PKC-α activity and that subsequently increased p(38)MAPK phosphorylation. Pretreatment with Go6976 (PKC-α inhibitor) and SB203580 (p(38)MAPK inhibitor) eliminated ONOO(-) caused inhibition on isoproterenol stimulated adenyl cyclase activity.
View Article and Find Full Text PDFWe have recently reported that treatment of bovine pulmonary artery smooth muscle cells with the thromboxane A(2) mimetic, U46619 stimulated NADPH oxidase derived O(2)(·-) level, which subsequently caused marked increase in [Ca(2+)](i)[17]. Herein, we demonstrated that O(2)(·-)-mediated increase in [Ca(2+)](i) stimulates an aprotinin sensitive proteinase activity, which proteolytically activates PKC-α under U46619 treatment to the cells. The activated PKC-α then phosphorylates p(38)MAPK and that subsequently caused G(i)α phosphorylation leading to stimulation of cPLA(2) activity in the cell membrane.
View Article and Find Full Text PDFWe investigated the role of TGF-β1 and TNF-α in mediating the effect of IL-1β in activating proMMP-9 and proMMP-2, and the involvement of an aprotinin sensitive protease in this scenario in bovine pulmonary artery smooth muscle cells. IL-1β induces TGF-β1 mediated stimulation of 92kDa proMMP-9 and 72kDa proMMP-2 mRNA and protein expression; whereas, the elevated level of TNF-α promotes activation of proMMP-9 and proMMP-2. Interestingly, TNF-α induced activation of proMMP-9 appeared to be mediated via a 43kDa aprotinin sensitive protease.
View Article and Find Full Text PDFCalpain system is generally known to be comprised of three molecules: two Ca2+-dependent proteases: mu- and m-calpains, and their endogenous inhibitor, calpastatin. While calpains have previously been considered as the cytoplasmic enzymes, research in the recent past demonstrated that mu-calpain, m-calpain and calpain 10 are present in mitochondria, which play important roles in a variety of pathophysiological conditions including necrotic and apoptotic cell death phenomena. Although a number of original research articles on mitochondrial calpain system are available, yet to the best of our knowledge, a precise review article on mitochondrial calpain system has, however, not been available.
View Article and Find Full Text PDFTreatment of bovine pulmonary smooth muscle cells with the TxA(2) mimetic, U46619 stimulated [Ca(2+)](i), which was inhibited upon pretreatment with apocynin (NADPH oxidase inhibitor). Pretreatment with cromakalim (K(V) channel opener) or nifedepine (L-VOCC inhibitor) inhibited U46619 induced increase in [Ca(2+)](i), indicating a role of K(V)-LVOCC axis in this scenario. Neither cromakalim nor nifedepine inhibited U46619 induced increase in NADPH oxidase activity, suggesting that the NADPH oxidase activation is proximal to the K(V)-LVOCC axis in the cells.
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