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Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis

Leptin is a type of adipokine mainly produced by adipocytes and reported to be overproduced in prostate cancer. However, it is not known whether it stimulates the proliferation of prostate cells. In this study, we investigated whether benign prostatic hyperplasia epithelial cells (BPH-1 cells) infec...

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Autores principales: Kim, Jung-Hyun, Han, Ik-Hwan, Shin, Su-Jin, Park, Sung-Yul, Chung, Hyo-Yeoung, Ryu, Jae-Sook
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Parasitology and Tropical Medicine 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8255495/
https://www.ncbi.nlm.nih.gov/pubmed/34218595
http://dx.doi.org/10.3347/kjp.2021.59.3.235
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author Kim, Jung-Hyun
Han, Ik-Hwan
Shin, Su-Jin
Park, Sung-Yul
Chung, Hyo-Yeoung
Ryu, Jae-Sook
author_facet Kim, Jung-Hyun
Han, Ik-Hwan
Shin, Su-Jin
Park, Sung-Yul
Chung, Hyo-Yeoung
Ryu, Jae-Sook
author_sort Kim, Jung-Hyun
collection PubMed
description Leptin is a type of adipokine mainly produced by adipocytes and reported to be overproduced in prostate cancer. However, it is not known whether it stimulates the proliferation of prostate cells. In this study, we investigated whether benign prostatic hyperplasia epithelial cells (BPH-1 cells) infected with Trichomonas vaginalis induced the proliferation of prostate cells via a leptin signaling pathway. To investigate the effect of crosstalk between adipocyte leptin and inflamed epithelial cell in proliferation of prostate cells, adipocytes 3T3-L1 cells were incubated in conditioned medium of BPH-1 cells infected with T. vaginalis (T. vaginalis-conditioned medium, TCM), and then the adipocyte-conditioned medium (ATCM) was identified to cause proliferation of prostate cells. BPH-1 cells incubated with live T. vaginalis released pro-inflammatory cytokines, and conditioned medium of these cells caused migration of adipocytes. When prostate stromal cells and BPH-1 cells were incubated with adipocyte conditioned medium containing leptin, their growth rates increased as did expression of the leptin receptor (known as OBR) and signaling molecules such as JAK2/STAT3, Notch and survivin. Moreover, blocking the OBR reduced this proliferation and the expression of leptin signaling molecules in response to ATCM. In conclusion, our findings show that inflamed BPH-1 cells infected with T. vaginalis induce the proliferation of prostate cells through leptin-OBR signaling. Therefore, it is likely that T. vaginalis contributes to prostate enlargement in BPH via adipocyte leptin released as a result of inflammation of the prostate.
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spelling pubmed-82554952021-07-15 Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis Kim, Jung-Hyun Han, Ik-Hwan Shin, Su-Jin Park, Sung-Yul Chung, Hyo-Yeoung Ryu, Jae-Sook Korean J Parasitol Original Article Leptin is a type of adipokine mainly produced by adipocytes and reported to be overproduced in prostate cancer. However, it is not known whether it stimulates the proliferation of prostate cells. In this study, we investigated whether benign prostatic hyperplasia epithelial cells (BPH-1 cells) infected with Trichomonas vaginalis induced the proliferation of prostate cells via a leptin signaling pathway. To investigate the effect of crosstalk between adipocyte leptin and inflamed epithelial cell in proliferation of prostate cells, adipocytes 3T3-L1 cells were incubated in conditioned medium of BPH-1 cells infected with T. vaginalis (T. vaginalis-conditioned medium, TCM), and then the adipocyte-conditioned medium (ATCM) was identified to cause proliferation of prostate cells. BPH-1 cells incubated with live T. vaginalis released pro-inflammatory cytokines, and conditioned medium of these cells caused migration of adipocytes. When prostate stromal cells and BPH-1 cells were incubated with adipocyte conditioned medium containing leptin, their growth rates increased as did expression of the leptin receptor (known as OBR) and signaling molecules such as JAK2/STAT3, Notch and survivin. Moreover, blocking the OBR reduced this proliferation and the expression of leptin signaling molecules in response to ATCM. In conclusion, our findings show that inflamed BPH-1 cells infected with T. vaginalis induce the proliferation of prostate cells through leptin-OBR signaling. Therefore, it is likely that T. vaginalis contributes to prostate enlargement in BPH via adipocyte leptin released as a result of inflammation of the prostate. The Korean Society for Parasitology and Tropical Medicine 2021-06 2021-06-30 /pmc/articles/PMC8255495/ /pubmed/34218595 http://dx.doi.org/10.3347/kjp.2021.59.3.235 Text en © 2021, Korean Society for Parasitology and Tropical Medicine https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Kim, Jung-Hyun
Han, Ik-Hwan
Shin, Su-Jin
Park, Sung-Yul
Chung, Hyo-Yeoung
Ryu, Jae-Sook
Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis
title Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis
title_full Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis
title_fullStr Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis
title_full_unstemmed Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis
title_short Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis
title_sort signaling role of adipocyte leptin in prostate cell proliferation induced by trichomonas vaginalis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8255495/
https://www.ncbi.nlm.nih.gov/pubmed/34218595
http://dx.doi.org/10.3347/kjp.2021.59.3.235
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