The Effect of Adiponectin on the Regulation of Filaggrin Expression in Normal Human Epidermal Keratinocytes
Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation. This study aimed to investigate the effect of adiponectin on the ex...
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| Published in | Annals of dermatology Vol. 30; no. 6; pp. 645 - 652 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
The Korean Dermatological Association; The Korean Society for Investigative Dermatology
01.12.2018
대한피부과학회 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1013-9087 2005-3894 2005-3894 |
| DOI | 10.5021/ad.2018.30.6.645 |
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| Abstract | Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation.
This study aimed to investigate the effect of adiponectin on the expression of
(FLG) in normal human epidermal keratinocytes (NHEKs).
NHEKs were serum-starved for 6h before being treated with adiponectin. Afterward, cell viability was assessed by MTT assay. We also treated with calcium, interleukin (IL)-4, and IL-13 to provide positive and negative comparative controls, respectively. Gene mRNA expression was quantified using real time reverse transcription polymerase chain reaction, and protein expression was evaluated using Western blot. To evaluate the relationship among mitogen-activated protein kinases (MAPKs), activator protein 1 (AP-1), and FLG, we also treated cells with inhibitors for MAPKs JNK, p38, and ERK1/2.
and
mRNA expression in NHEKs significantly increased after treatment with 10 µg/ml adiponectin. Adiponectin also restored
and
mRNA expression that was otherwise inhibited by treatment with IL-4 and IL-13. Adiponectin induced
expression via AP-1 and MAPK signaling.
Adiponectin positively regulated the expression of
and could be useful as a therapeutic agent to control diseases related to disrupted skin barrier function. |
|---|---|
| AbstractList | Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation.
This study aimed to investigate the effect of adiponectin on the expression of
(FLG) in normal human epidermal keratinocytes (NHEKs).
NHEKs were serum-starved for 6h before being treated with adiponectin. Afterward, cell viability was assessed by MTT assay. We also treated with calcium, interleukin (IL)-4, and IL-13 to provide positive and negative comparative controls, respectively. Gene mRNA expression was quantified using real time reverse transcription polymerase chain reaction, and protein expression was evaluated using Western blot. To evaluate the relationship among mitogen-activated protein kinases (MAPKs), activator protein 1 (AP-1), and FLG, we also treated cells with inhibitors for MAPKs JNK, p38, and ERK1/2.
and
mRNA expression in NHEKs significantly increased after treatment with 10 µg/ml adiponectin. Adiponectin also restored
and
mRNA expression that was otherwise inhibited by treatment with IL-4 and IL-13. Adiponectin induced
expression via AP-1 and MAPK signaling.
Adiponectin positively regulated the expression of
and could be useful as a therapeutic agent to control diseases related to disrupted skin barrier function. Background: Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation. Objective: This study aimed to investigate the effect of adiponectin on the expression of filaggrin (FLG) in normal human epidermal keratinocytes (NHEKs). Methods: NHEKs were serum-starved for 6h before being treated with adiponectin. Afterward, cell viability was assessed by MTT assay. We also treated with calcium, interleukin (IL)-4, and IL-13 to provide positive and negative comparative controls, respectively. Gene mRNA expression was quantified using real time reverse transcription polymerase chain reaction, and protein expression was evaluated using Western blot. To evaluate the relationship among mitogen-activated protein kinases (MAPKs), activator protein 1 (AP-1), and FLG, we also treated cells with inhibitors for MAPKs JNK, p38, and ERK1/2. Results: FLG and FLG-2 mRNA expression in NHEKs significantly increased after treatment with 10 μg/ml adiponectin. Adiponectin also restored FLG and FLG-2 mRNA expression that was otherwise inhibited by treatment with IL-4 and IL-13. Adiponectin induced FLG expression via AP-1 and MAPK signaling. Conclusion: Adiponectin positively regulated the expression of FLG and could be useful as a therapeutic agent to control diseases related to disrupted skin barrier function. KCI Citation Count: 1 Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation.BACKGROUNDAdiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation.This study aimed to investigate the effect of adiponectin on the expression of filaggrin (FLG) in normal human epidermal keratinocytes (NHEKs).OBJECTIVEThis study aimed to investigate the effect of adiponectin on the expression of filaggrin (FLG) in normal human epidermal keratinocytes (NHEKs).NHEKs were serum-starved for 6h before being treated with adiponectin. Afterward, cell viability was assessed by MTT assay. We also treated with calcium, interleukin (IL)-4, and IL-13 to provide positive and negative comparative controls, respectively. Gene mRNA expression was quantified using real time reverse transcription polymerase chain reaction, and protein expression was evaluated using Western blot. To evaluate the relationship among mitogen-activated protein kinases (MAPKs), activator protein 1 (AP-1), and FLG, we also treated cells with inhibitors for MAPKs JNK, p38, and ERK1/2.METHODSNHEKs were serum-starved for 6h before being treated with adiponectin. Afterward, cell viability was assessed by MTT assay. We also treated with calcium, interleukin (IL)-4, and IL-13 to provide positive and negative comparative controls, respectively. Gene mRNA expression was quantified using real time reverse transcription polymerase chain reaction, and protein expression was evaluated using Western blot. To evaluate the relationship among mitogen-activated protein kinases (MAPKs), activator protein 1 (AP-1), and FLG, we also treated cells with inhibitors for MAPKs JNK, p38, and ERK1/2.FLG and FLG-2 mRNA expression in NHEKs significantly increased after treatment with 10 µg/ml adiponectin. Adiponectin also restored FLG and FLG-2 mRNA expression that was otherwise inhibited by treatment with IL-4 and IL-13. Adiponectin induced FLG expression via AP-1 and MAPK signaling.RESULTSFLG and FLG-2 mRNA expression in NHEKs significantly increased after treatment with 10 µg/ml adiponectin. Adiponectin also restored FLG and FLG-2 mRNA expression that was otherwise inhibited by treatment with IL-4 and IL-13. Adiponectin induced FLG expression via AP-1 and MAPK signaling.Adiponectin positively regulated the expression of FLG and could be useful as a therapeutic agent to control diseases related to disrupted skin barrier function.CONCLUSIONAdiponectin positively regulated the expression of FLG and could be useful as a therapeutic agent to control diseases related to disrupted skin barrier function. |
| Author | Seo, Seong Jun Park, Kui Young Ahn, Ga Ram Choi, Sun Young Kim, Min Jeong Lee, Mi-Kyung |
| AuthorAffiliation | 2 Department of Laboratory Medicine, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea Department of Dermatology, Inje University Seoul Paik Hospital, Inje University College of Medicine, Seoul, Korea 1 Department of Dermatology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea |
| AuthorAffiliation_xml | – name: 1 Department of Dermatology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea – name: Department of Dermatology, Inje University Seoul Paik Hospital, Inje University College of Medicine, Seoul, Korea – name: 2 Department of Laboratory Medicine, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea |
| Author_xml | – sequence: 1 givenname: Sun Young surname: Choi fullname: Choi, Sun Young organization: Department of Dermatology, Inje University Seoul Paik Hospital, Inje University College of Medicine, Seoul, Korea – sequence: 2 givenname: Min Jeong surname: Kim fullname: Kim, Min Jeong organization: Department of Dermatology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea – sequence: 3 givenname: Ga Ram surname: Ahn fullname: Ahn, Ga Ram organization: Department of Dermatology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea – sequence: 4 givenname: Kui Young orcidid: 0000-0001-5965-1754 surname: Park fullname: Park, Kui Young organization: Department of Dermatology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea – sequence: 5 givenname: Mi-Kyung surname: Lee fullname: Lee, Mi-Kyung organization: Department of Laboratory Medicine, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea – sequence: 6 givenname: Seong Jun orcidid: 0000-0003-2915-839X surname: Seo fullname: Seo, Seong Jun organization: Department of Dermatology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea |
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| Copyright | Copyright © 2018 The Korean Dermatological Association and The Korean Society for Investigative Dermatology. Copyright © 2018 The Korean Dermatological Association and The Korean Society for Investigative Dermatology 2018 The Korean Dermatological Association and The Korean Society for Investigative Dermatology |
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| Keywords | Keratinocytes Filaggrin Cell differentiation Transcription factor AP-1 Adiponectin Mitogen-activated protein kinases |
| Language | English |
| License | Copyright © 2018 The Korean Dermatological Association and The Korean Society for Investigative Dermatology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://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. |
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| Snippet | Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies... Background: Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent... |
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| Title | The Effect of Adiponectin on the Regulation of Filaggrin Expression in Normal Human Epidermal Keratinocytes |
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| ispartofPNX | Annals of Dermatology, 2018, 30(6), , pp.645-652 |
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