Expression of Nicotinic Acetylcholine Receptors in Pulmonary Artery Endothelial and Smooth Muscle Cells

Publication Date

July 2019

Location

LSU Health Medical Education Building

Document Type

Abstract

Start Date

26-7-2019 9:00 AM

End Date

26-7-2019 12:00 PM

Description

Nicotinic acetylcholine receptors (nAChRs) mediate the body’s response to nicotine; expression of these receptors defines the tissue and organ specific response to nicotine. Previous studies from our lab show that in mice chronic nicotine inhalation leads to pulmonary vascular remodeling and increased right ventricular systolic pressure. The aim of the current study is to identify the nAChRs that are expressed by the pulmonary vasculature, including pulmonary artery endothelial cells (PAEC) and smooth muscle cells (PASMC). Using quantitative real time polymerase chain reaction (qRT-PCR), we looked at relative mRNA expression of α3-, α4-, α7-, and α9-nAChR in human PAEC and PASMC. These receptors were chosen because α7 and α9 have been shown to be involved in many signaling pathways, α3 is involved in nicotine-induced carcinogenesis, and α4 is involved in nicotine-induced addiction. In addition, we used immunohistochemistry (IHC) on mouse lung tissue sections to detect α7. QRT-PCR results showed that HPAEC predominantly express α7, and HPASMC express α3, α7, and α9 with α3 being expressed at the highest level followed by α7. Further, IHC on lung tissue sections showed that α7 is prevalent in the smooth muscle cells and epithelial cells, however expression in the endothelial cells is unclear. Our future direction is to examine the functional role of α7-nAChR in PAEC, and the role of both α7 and α3 in PASMC in nicotine induced vascular remodeling in vitro and in vivo.

Comments

Mentor: Dr. Xinping Yue

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Jul 26th, 9:00 AM Jul 26th, 12:00 PM

Expression of Nicotinic Acetylcholine Receptors in Pulmonary Artery Endothelial and Smooth Muscle Cells

LSU Health Medical Education Building

Nicotinic acetylcholine receptors (nAChRs) mediate the body’s response to nicotine; expression of these receptors defines the tissue and organ specific response to nicotine. Previous studies from our lab show that in mice chronic nicotine inhalation leads to pulmonary vascular remodeling and increased right ventricular systolic pressure. The aim of the current study is to identify the nAChRs that are expressed by the pulmonary vasculature, including pulmonary artery endothelial cells (PAEC) and smooth muscle cells (PASMC). Using quantitative real time polymerase chain reaction (qRT-PCR), we looked at relative mRNA expression of α3-, α4-, α7-, and α9-nAChR in human PAEC and PASMC. These receptors were chosen because α7 and α9 have been shown to be involved in many signaling pathways, α3 is involved in nicotine-induced carcinogenesis, and α4 is involved in nicotine-induced addiction. In addition, we used immunohistochemistry (IHC) on mouse lung tissue sections to detect α7. QRT-PCR results showed that HPAEC predominantly express α7, and HPASMC express α3, α7, and α9 with α3 being expressed at the highest level followed by α7. Further, IHC on lung tissue sections showed that α7 is prevalent in the smooth muscle cells and epithelial cells, however expression in the endothelial cells is unclear. Our future direction is to examine the functional role of α7-nAChR in PAEC, and the role of both α7 and α3 in PASMC in nicotine induced vascular remodeling in vitro and in vivo.