Ashish Misra

Ashish Misra
Heart Research Institute | HRI

PhD.

About

30
Publications
6,900
Reads
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606
Citations
Citations since 2016
22 Research Items
520 Citations
2016201720182019202020212022020406080100120140
2016201720182019202020212022020406080100120140
2016201720182019202020212022020406080100120140
2016201720182019202020212022020406080100120140
Additional affiliations
December 2011 - present
Yale University
Position
  • PostDoc Position
Description
  • Vascular Biology and Therapeutics
January 2006 - March 2011
Nanyang Technological University

Publications

Publications (30)
Article
Full-text available
Clonal expansion is a process that can drive pathogenesis in human diseases, with atherosclerosis being a prominent example. Despite advances in understanding the etiology of atherosclerosis, clonality studies of vascular cells remain in an early stage. Recently, several paradigm-shifting preclinical studies have identified clonal expansion of prog...
Article
Full-text available
Obstructive arterial diseases including supravalvular aortic stenosis (SVAS), atherosclerosis and restenosis share two important features: an abnormal or disrupted elastic lamellae structure and excessive smooth muscle cells (SMCs). However, the relationship between these pathological features is poorly delineated. SVAS is caused by heterozygous lo...
Article
Full-text available
Mural cells collectively refer to the smooth muscle cells and pericytes of the vasculature. This heterogenous population of cells play a crucial role in the regulation of blood pressure, distribution, and the structural integrity of the vascular wall. As such, dysfunction of mural cells can lead to the pathogenesis and progression of a number of di...
Article
Full-text available
Deciphering the origins of the various cells in atherosclerotic plaques, the regulation of their fates and their functions is an essential step towards developing strategies to limit or even reverse disease progression to myocardial infarction. In this issue, Newman et al. advance our understanding of the roles of non-vascular smooth muscle cells i...
Article
Full-text available
Colchicine, an inexpensive immunomodulatory drug used traditionally to treat gout and familial Mediterranean fever, is rapidly accumulating basic and clinical evidence for a therapeutic role in atherosclerotic cardiovascular disease. Its athero-protective properties are thought to be mainly related to its effect on tubulin polymerisation, enabling...
Article
Full-text available
Background Release of neutrophil extracellular traps (NETs) after percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) is associated with periprocedural myocardial infarction, as a result of microvascular obstruction via pro‐inflammatory and prothrombotic pathways. Colchicine is a well‐established anti‐inflammatory agent with g...
Article
Many type 2 diabetes patients develop cardiovascular disease (CVD) while some are protected. Toyohara et al. (2020) find that elevated arylacetamide deacetylase (AADAC) expression in vascular smooth muscle cells (dVSMCs) differentiated from patient-derived induced pluripotent stem cells is associated with cardioprotection. AADAC overexpression alte...
Article
Circulating plasma TRAIL levels are suppressed in patients with cardiovascular and diabetic diseases. To identify novel targets in vascular metabolic diseases, genome-wide transcriptome of aortic tissue from Trail-/- vs. Trail+/+ mice were interrogated. We found 861 genes differentially expressed with TRAIL deletion. Gene enrichment analyses showed...
Preprint
Full-text available
Objective: Release of neutrophil extracellular traps (NETs) after percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) is associated with peri-procedural myocardial infarction, as a result of microvascular obstruction via pro-inflammatory and pro-thrombotic pathways. Colchicine is a potent, well-established anti-inflammatory ag...
Article
Purpose: Existing literature reports that colchicine inhibits inflammasome activation and downstream inflammatory cytokine production and stabilizes coronary plaque. However, colchicine's effect on chemokines, which orchestrate multiple atheroinflammatory pathways, is unknown. Methods: Patients with acute coronary syndrome (ACS) were randomly as...
Article
Atherosclerosis is now considered a chronic maladaptive inflammatory disease. The hallmark feature both in human and murine disease are atherosclerotic plaques. Macrophages and various T-cell lineages play a crucial role in atherosclerotic plaque establishment and disease progression. Humans and mice share many of the same processes that occur with...
Article
Full-text available
Smooth muscle cells (SMCs) play a key role in atherogenesis. However, mechanisms regulating expansion and fate of pre-existing SMCs in atherosclerotic plaques remain poorly defined. Here we show that multiple SMC progenitors mix to form the aorta during development. In contrast, during atherogenesis, a single SMC gives rise to the smooth muscle-der...
Article
Full-text available
Smooth muscle cells (SMCs) play a key role in atherogenesis. However, mechanisms reg-ulating expansion and fate of pre-existing SMCs in atherosclerotic plaques remain poorlydefined. Here we show that multiple SMC progenitors mix to form the aorta during devel-opment. In contrast, during atherogenesis, a single SMC gives rise to the smooth muscle-de...
Article
Full-text available
The aorta is the largest artery in the body. The aortic wall is composed of an inner layer of endothelial cells, a middle layer of alternating elastic lamellae and smooth muscle cells (SMCs), and an outer layer of fibroblasts and extracellular matrix. In contrast to the widespread study of pathological models (e.g., atherosclerosis) in the adult ao...
Chapter
The vessel wall is composed of distinct cellular layers, yet communication among individual cells within and between layers results in a dynamic and versatile structure. The morphogenesis of the normal vascular wall involves a highly regulated process of cell proliferation, migration, and differentiation. The use of modern developmental biological...
Article
Full-text available
The aorta is the largest artery in the body, yet processes underlying aortic pathology are poorly understood. The arterial media consists of circumferential layers of elastic lamellae and smooth muscle cells (SMCs), and many arterial diseases are characterized by defective lamellae and excess SMCs; however, a mechanism linking these pathological fe...
Article
Full-text available
Excess and ectopic smooth muscle cells (SMCs) are central to cardiovascular disease pathogenesis, but underlying mechanisms are poorly defined. For instance, pulmonary hypertension (PH) or elevated pulmonary artery blood pressure is a devastating disease with distal extension of smooth muscle to normally unmuscularized pulmonary arterioles. We iden...
Article
Full-text available
Metastasis is a multi-step process which requires the conversion of polarized epithelial cells to mesenchymal cells, Epithelial-Mesenchymal Transition (EMT). EMT is essential during embryonic morphogenesis and has been implicated in the progression of primary tumors towards metastasis. Hypoxia is known to induce EMT; however the molecular mechanism...
Article
Full-text available
Remodeling of the membrane and cytoskeleton is involved in a wide range of normal and pathologic cellular function. These are complex, highly-coordinated biochemical and biophysical processes involving dozens of proteins. Serving as a scaffold for a variety of proteins and possessing a domain that interacts with plasma membranes, the BAR family of...
Article
Full-text available
N-WASP (Neural Wiskott Aldrich Syndrome Protein) regulates actin polymerization by activating the Arp2/3 complex and promotes the formation of actin-rich structures such as filopodia. Such actin-rich structures play critical roles in cell adhesion and cell motility. Analysis of the adhesion properties of N-WASP+/+ and N-WASP-/- mouse embryonic fibr...
Article
WASP (Wiskott-Aldrich syndrome protein) has been proposed to adopt a closed conformation (autoinhibited conformation) due to interaction between the carboxy terminal and the GTPase binding domain. Various WASP-interacting proteins have been suggested to relieve this autoinhibition. We have used the split YFP (Yellow Fluorescent Protein) to analyze...

Questions

Questions (2)
Question
I want to inhibit aplhavBeta3 integrin signaling in pregnant mouse.
Is that possible for me to give Cilengitide inhibitor of RGD motif to the pregnant female at E14.5 so that I can analyse the pups after the birth?
Question
I want to inhibit aplhavBeta3 integrin signaling in pregnant mouse. is that possible for me to give Cilengitide a inhibitor of RGD motif to the pregnant female at E14.5 so that I can analyse the pups after the birth.

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