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Assistant Professor Amarjit Mishra Contribution to the Field of Science

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Scientists from all over the world have been advancing civilization by conducting extensive research in the field of science. The contributions of a select few scientists in this setting are notable. The work of Amarjit Mishra has a distinct place in this regard. At Auburn University, Amarjit Mishra teaches as an assistant professor. His present study primarily focused on respiratory illnesses. Finding new regulatory pathways for lung disorders including pulmonary fibrosis, which causes severe, extensive alveolar damage, and acute respiratory distress syndrome (ARDS) is one of his main objectives.

Amarjit Mishra Assistant Professor at Auburn University Background

Amarjit Mishra Assistant Professor know for his dynamic knowledge. He completed a masters and doctorate in Veterinary medicine from India. Due to his keen interest and profound knowledge, Amarjit Mishra went on to complete a PhD (Doctor of Philosophy) from the Oklahoma Centre for Respiratory and Infectious Diseases (OCRID) in the Department of Physiological Sciences, Oklahoma State University of USA. In Oklahoma, OCRID serves as a focal center for growing research on infectious respiratory diseases. OCRID conducts important studies on respiratory infectious illnesses with a focus on COVID-19, respiratory syncytial virus, influenza virus, and respiratory bacterial and fungal infections. The interdisciplinary projects in OCRID include bioengineering, nutrition, disease etiology, diagnostics, and treatments. Amarjit Mishra previously held the prestigious positions of Research and Postdoctoral Fellow at the Cardiovascular and Pulmonary branch, NHLBI at the National Institute of Health in Maryland, USA, and Assistant Professor at Auburn University.

Understanding of the Pathophysiology by Amarjit Mishra

Amarjit Mishra has transformed the understanding of the pathophysiology of alveolar inflammation. The earlier work carried on by Amarjit Mishra, Auburn University has focused on understanding the cellular and molecular mechanisms of the cause of alveolar inflammation.

One of the major roles in the functioning of alveoli play from the pulmonary surfactants. Pulmonary surfactant, a complex of lipids and proteins lining the alveolar surface, is responsible for lowering surface tension at the air-liquid interface thereby preventing alveolar collapse at the end of expiration.

Despite being of significance, the mechanism of release of lung surfactant poorly understand. Thus, Amarjit Mishra, Auburn University and his team of researchers decided to study the implication of alveolar type I (AEC I) and type II (AEC II) epithelial cell-cell communications and microRNA function in lung surfactant release.

They confirmed that a certain category of receptors, known as purinergic P2X7 receptors are functionally active in AEC I. They also showed that the stimulation of P2X7 receptors in AEC I was responsible for the release of the energy currency, ATP. ATP is a soluble mediator which know to acti in a paracrine fashion on AEC II. His study has established that this communication between AEC I and AEC II is a physiologically relevant phenomenon to hyperventilation-induced surfactant release.

He was also able to bring forth the significant role of the P2X7 receptor in AEC I as an important regulator of surfactant secretion and AEC I and AEC II communications. This work publish in the Journal of Biomedical Sciences in 2013 in an article titled, “New insights of P2X7 receptor signaling pathway in alveolar functions.”

Amarjit Mishra has continued his research into the many processes that control alveolar inflammation after making this finding. The characteristics of Acute respiratory distress syndrome (ARDS) and pulmonary fibrosis include low blood oxygen levels and the inability to raise oxygen levels to normal levels.

However, the prevalent course of treatment principally focused on supportive lung-protective ventilation and fluid restriction without a deep understanding of the regulatory pathway responsible for it.

Thus, Amarjit Mishra focussed on finding regulatory pathways and the pathogenic function of these receptors. It finds that Purinergic P2X7 receptors find at the crucial intersection of cytokine regulation, neutrophil recruitment, and inflammation in the alveolar region.

Discovery in Science that Amarjit Mishra has Carried Out

Another discovery in science that was carried out by Amarjit Mishra with a team of able scientists concluded that miR-101 is an anti-fibrotic microRNA and a potential therapeutic target for pulmonary fibrosis. It was earlier known that Aberrant proliferation and activation of lung fibroblasts contribute to the initiation and progression of idiopathic pulmonary fibrosis (IPF). However, the mechanisms responsible for the proliferation and activation of fibroblasts was not fully understood.

The team of scientists thus decided to investigate the role of miR-101 in the proliferation and activation of lung fibroblasts. For this study, miR-101 expression was determined in lung tissues from patients with IPF and mice with bleomycin-induced pulmonary fibrosis.

The regulation of miR-101 and cellular signaling was investigated in pulmonary fibroblasts in vitro The role of miR-101 in pulmonary fibrosis in vivo was studied using adenovirus-mediated gene transfer in mice. The expression of miR-101 was down-regulated in fibrotic lungs from patients with IPF and bleomycin-treated mice.

It was found that the down-regulation of miR-101 occurred via the E26 transformation-specific (ETS) transcription factor. miR-101 suppressed the WNT5a-induced proliferation of lung fibroblasts by inhibiting NFATc2 signaling via targeting Frizzled receptor 4/6 and the TGF-β-induced activation of lung fibroblasts by inhibition of SMAD2/3 signaling via targeting the TGF-β receptor 1.

Adenovirus-mediated miR-101 gene transfer in the mouse lung attenuated bleomycin-induced lung fibrosis and improved lung function. Thus proving potency of miR-101 as a potential therapeutic target for pulmonary fibrosis.
Dendritic cell function in allergic asthma has also been identified by Amarjit Mishra, who has made scientific advancements in this area. He has found that T-helper cells play a significant role in allergic asthma, so it is important to emphasize the fact that asthma is also known as T helper type 2 sickness of the airways.

In his investigation, he was able to identify specific dendritic cell-related pathways. He studied the immunological response triggered by these dendritic cells in great detail. He has also investigated how the very low density lipoprotein receptor (VLDLr) and LDL receptor related protein-1 affect the function of dendritic cells in controlling the immune response in allergic asthma (LRP-1). Amarjit Mishra has been putting in endless effort to better comprehend the causative relationship between the dendritic cells and allergic asthma.
Science has advanced much thanks to the contributions of researchers like Amarjit Mishra from Auburn University, and in the future it will be important to give them more credit for their work.

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