Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway
Aim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with...
Saved in:
| Main Authors: | , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2019-01-01
|
| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2019/8512028 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832552135306248192 |
|---|---|
| author | Cuiping Liu Ludan Qin Jingya Ding Luping Zhou Chenlin Gao Ting Zhang Man Guo Wei Huang Zongzhe Jiang Yang Long Yong Xu |
| author_facet | Cuiping Liu Ludan Qin Jingya Ding Luping Zhou Chenlin Gao Ting Zhang Man Guo Wei Huang Zongzhe Jiang Yang Long Yong Xu |
| author_sort | Cuiping Liu |
| collection | DOAJ |
| description | Aim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes mellitus (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed by flow cytometry and ELISA. The expression of transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen1, IL-4Rα, and IL-13Rα1 in renal tubular epithelial cells (HK-2) induced by IL-4, IL-13, or high glucose was analyzed by ELISA or qPCR. Results. The proportion of ILC2s and the levels of IL-4, IL-5, and IL-13 were significantly increased in DKD patients and were positively correlated with the severity of DKD (P<0.05). The expression of TGF-β1, FN, and collagen1 was significantly upregulated in HK-2 cells induced by IL-4 or IL-13 (P<0.05). Moreover, the IL-4Rα and IL-13Rα1 mRNA in HK2 cells were increased followed by high glucose alone or combined with IL-4 or IL-13, but the differences were not statistically significant (P>0.05). However, compared with high-glucose stimulation alone, the expression of TGF-β1, FN, and collagen1 was significantly increased in HK-2 cells induced by high glucose combined with IL-4 or IL-13 (P<0.05). Conclusions. ILC2s may participate in renal fibrosis in DKD partly via TGF-β1 signal pathway. |
| format | Article |
| id | doaj-art-109349dc60c7480a85cad985bf5e5d9e |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-109349dc60c7480a85cad985bf5e5d9e2025-02-03T05:59:20ZengWileyJournal of Diabetes Research2314-67452314-67532019-01-01201910.1155/2019/85120288512028Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal PathwayCuiping Liu0Ludan Qin1Jingya Ding2Luping Zhou3Chenlin Gao4Ting Zhang5Man Guo6Wei Huang7Zongzhe Jiang8Yang Long9Yong Xu10Luzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaDepartment of Endocrinology, Zigong Fourth People’s Hospital, Zigong, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaLuzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, ChinaAim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes mellitus (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed by flow cytometry and ELISA. The expression of transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen1, IL-4Rα, and IL-13Rα1 in renal tubular epithelial cells (HK-2) induced by IL-4, IL-13, or high glucose was analyzed by ELISA or qPCR. Results. The proportion of ILC2s and the levels of IL-4, IL-5, and IL-13 were significantly increased in DKD patients and were positively correlated with the severity of DKD (P<0.05). The expression of TGF-β1, FN, and collagen1 was significantly upregulated in HK-2 cells induced by IL-4 or IL-13 (P<0.05). Moreover, the IL-4Rα and IL-13Rα1 mRNA in HK2 cells were increased followed by high glucose alone or combined with IL-4 or IL-13, but the differences were not statistically significant (P>0.05). However, compared with high-glucose stimulation alone, the expression of TGF-β1, FN, and collagen1 was significantly increased in HK-2 cells induced by high glucose combined with IL-4 or IL-13 (P<0.05). Conclusions. ILC2s may participate in renal fibrosis in DKD partly via TGF-β1 signal pathway.http://dx.doi.org/10.1155/2019/8512028 |
| spellingShingle | Cuiping Liu Ludan Qin Jingya Ding Luping Zhou Chenlin Gao Ting Zhang Man Guo Wei Huang Zongzhe Jiang Yang Long Yong Xu Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway Journal of Diabetes Research |
| title | Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway |
| title_full | Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway |
| title_fullStr | Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway |
| title_full_unstemmed | Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway |
| title_short | Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway |
| title_sort | group 2 innate lymphoid cells participate in renal fibrosis in diabetic kidney disease partly via tgf β1 signal pathway |
| url | http://dx.doi.org/10.1155/2019/8512028 |
| work_keys_str_mv | AT cuipingliu group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT ludanqin group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT jingyading group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT lupingzhou group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT chenlingao group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT tingzhang group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT manguo group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT weihuang group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT zongzhejiang group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT yanglong group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway AT yongxu group2innatelymphoidcellsparticipateinrenalfibrosisindiabetickidneydiseasepartlyviatgfb1signalpathway |