Monoamine Oxidase Deficiency Causes Prostate Atrophy and Reduces Prostate Progenitor Cell Activity

Lijuan Yin; Jingjing Li; Chun-Peng Liao; Boyang Jason Wu

doi:10.1002/stem.2831

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Monoamine Oxidase Deficiency Causes Prostate Atrophy and Reduces Prostate Progenitor Cell Activity

Journal article

Open access

Peer reviewed

Monoamine Oxidase Deficiency Causes Prostate Atrophy and Reduces Prostate Progenitor Cell Activity

Lijuan Yin, Jingjing Li, Chun-Peng Liao and Boyang Jason Wu

Stem cells (Dayton, Ohio), Vol.36(8), pp.1249-1258

08/2018

DOI: https://doi.org/10.1002/stem.2831

PMID: 29637670

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Abstract

Atrophy

Cell Line

Cell Proliferation - drug effects

Epithelial Cells - drug effects

Epithelial Cells - metabolism

Epithelial Cells - pathology

Gene Silencing - drug effects

Humans

Mice, Knockout

Monoamine Oxidase - deficiency

Monoamine Oxidase Inhibitors - pharmacology

Organ Size - drug effects

Prostate - drug effects

Prostate - enzymology

Prostate - pathology

RNA, Small Interfering - metabolism

Spheroids, Cellular - drug effects

Spheroids, Cellular - metabolism

Spheroids, Cellular - pathology

Stem Cells - drug effects

Stem Cells - metabolism

Hyperplasia

Monoamine oxidases (MAOs) degrade a number of biogenic and dietary amines, including monoamine neurotransmitters, and play an essential role in many biological processes. Neurotransmitters and related neural events have been shown to participate in the development, differentiation, and maintenance of diverse tissues and organs by regulating the specialized cellular function and morphological structures of innervated organs such as the prostate. Here we show that mice lacking both MAO isoforms, MAOA and MAOB, exhibit smaller prostate mass and develop epithelial atrophy in the ventral and dorsolateral prostates. The cellular composition of prostate epithelium showed reduced CK5 or p63 basal cells, accompanied by lower Sca-1 expression in p63 basal cells, but intact differentiated CK8 luminal cells in MAOA/B-deficient mouse prostates. MAOA/B ablation also decreased epithelial cell proliferation without affecting cell apoptosis in mouse prostates. Using a human prostate epithelial cell line, we found that stable knockdown of MAOA and MAOB impaired the capacity of prostate stem cells to form spheres, coinciding with a reduced CD133 /CD44 /CD24 stem cell population and less expression of CK5 and select stem cell markers, including ALDH1A1, TROP2, and CD166. Alternative pharmacological inhibition of MAOs also repressed prostate cell stemness. In addition, we found elevated expression of MAOA and MAOB in epithelial and/or stromal components of human prostate hyperplasia samples compared with normal prostate tissues. Taken together, our findings reveal critical roles for MAOs in the regulation of prostate basal progenitor cells and prostate maintenance. Stem Cells 2018;36:1249-1258.

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Title: Monoamine Oxidase Deficiency Causes Prostate Atrophy and Reduces Prostate Progenitor Cell Activity
Creators: Lijuan Yin - Sichuan University
Jingjing Li - Washington State University Spokane
Chun-Peng Liao - Lawrence J. Ellison Institute for Transformative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA
Boyang Jason Wu (Author) - Washington State University Spokane
Publication Details: Stem cells (Dayton, Ohio), Vol.36(8), pp.1249-1258
Academic Unit: Pharmacy and Pharmaceutical Sciences, College of
Identifiers: 99900620489701842
Language: English
Resource Type: Journal article