Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury
Background : Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI....
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| Format: | Article |
| Language: | English |
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The Korean Society of Nephrology
2018-03-01
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| Series: | Kidney Research and Clinical Practice |
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| Online Access: | https://doi.org/10.23876/j.krcp.2018.37.1.30 |
| _version_ | 1818035427531030528 |
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| author | Jong Hwan Jung Jee Eun Choi Ju Hung Song Seon-Ho Ahn |
| author_facet | Jong Hwan Jung Jee Eun Choi Ju Hung Song Seon-Ho Ahn |
| author_sort | Jong Hwan Jung |
| collection | DOAJ |
| description | Background : Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI. Methods : Pax8-rtTA/tetracycline response element-human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI. Results : Results of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the collagen 3a1 gene in folic acid-treated transgenic mice overexpressing human CD 36 compared with folic acid-treated wild type mice. Conclusion : Human CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease. |
| first_indexed | 2024-12-10T06:54:53Z |
| format | Article |
| id | doaj.art-263c12a680dc4c2aa6434cf8c5a2f106 |
| institution | Directory Open Access Journal |
| issn | 2211-9132 |
| language | English |
| last_indexed | 2024-12-10T06:54:53Z |
| publishDate | 2018-03-01 |
| publisher | The Korean Society of Nephrology |
| record_format | Article |
| series | Kidney Research and Clinical Practice |
| spelling | doaj.art-263c12a680dc4c2aa6434cf8c5a2f1062022-12-22T01:58:28ZengThe Korean Society of NephrologyKidney Research and Clinical Practice2211-91322018-03-01371304010.23876/j.krcp.2018.37.1.30j.krcp.2018.37.1.30Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injuryJong Hwan Jung0Jee Eun Choi1Ju Hung Song2Seon-Ho Ahn3Division of Nephrology, Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, KoreaDivision of Nephrology, Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, KoreaDivision of Nephrology, Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, KoreaDivision of Nephrology, Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, KoreaBackground : Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI. Methods : Pax8-rtTA/tetracycline response element-human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI. Results : Results of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the collagen 3a1 gene in folic acid-treated transgenic mice overexpressing human CD 36 compared with folic acid-treated wild type mice. Conclusion : Human CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease.https://doi.org/10.23876/j.krcp.2018.37.1.30Acute kidney injuryFibrosisFolic acidRenal insufficiency |
| spellingShingle | Jong Hwan Jung Jee Eun Choi Ju Hung Song Seon-Ho Ahn Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury Kidney Research and Clinical Practice Acute kidney injury Fibrosis Folic acid Renal insufficiency |
| title | Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury |
| title_full | Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury |
| title_fullStr | Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury |
| title_full_unstemmed | Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury |
| title_short | Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury |
| title_sort | human cd36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid induced acute kidney injury |
| topic | Acute kidney injury Fibrosis Folic acid Renal insufficiency |
| url | https://doi.org/10.23876/j.krcp.2018.37.1.30 |
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