The Role of Long Non-Coding RNAs in the Progression of Renal Fibrosis.

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Abstract Title

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TAKUJI

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ISHIMOTO

Co-author 1

Kentaro Imai imai24@med.nagoya-u.ac.jp Nagoya University Nephrology Nagoya

Co-author 2

Kazuhiro Furuhashi furu13@med.nagoya-u.ac.jp Nagoya University Nephrology Nagoya

Co-author 3

Yasuhiko Ito yasuito@aichi-med-u.ac.jp Aichi Medical University Nephrology and Rheumatology Nagakute

Co-author 4

Shoichi Maruyama marus@med.nagoya-u.ac.jp Nagoya University Nephrology Nagoya

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Introduction

Renal interstitial fibrosis is a common response to injury or chronic damage to the kidney and is a major contributor to the progression of chronic kidney diseases. Effective treatment strategies for renal interstitial fibrosis are not yet firmly established, making it a challenging aspect of managing kidney diseases. Long non-coding RNAs (lncRNAs) are non-protein encoding RNAs composed of more than 200 nucleotides. They play roles in diverse physiological and pathological processes, including transcriptional regulation, epigenetic modification, cellular signaling, and the development of various diseases. However, the roles of lncRNAs in the progression of renal diseases, including renal interstitial fibrosis, are poorly understood.

Methods

Immortalized human proximal tubular cells (HK-2) and primary cultured human renal proximal tubular epithelial cells (RPTECs) were stimulated by transforming growth factor–β1 (TGF-β1) or hypoxia. Using microarray assays, upregulation of the expressions of the lncRNAs lnc-CHAF1B-3 and CASC15 was observed. The roles of these lncRNAs were assessed using antisense oligonucleotides (ASOs) and siRNAs. Additionally, qRT-PCR analyses were performed on paraffin-embedded kidney biopsy samples from various kidney diseases, including IgA nephropathy.

Results

Suppression of Lnc-CHAF1B-3 significantly reduced TGF-β1-induced upregulation of collagen type I alpha 1, Cadherin-2, Plasminogen Activator Inhibitor-1, Snail Family Transcriptional Repressor I (SNAI1), and SNAI2 expressions. qRT-PCR analyses of kidney biopsy samples from IgA nephropathy patients demonstrated a negative correlation between lnc-CHAF1B-3 expression and estimated glomerular filtration rate. Fluorescent in situ hybridization revealed that lnc-CHAF1B-3 is expressed in proximal tubules. Similar patterns were observed in the analyses of CASC15 expression.

Conclusions

Our findings suggest that both lnc-CHAF1B-3 and CASC15 are involved in the progression of renal fibrosis by regulating epithelial-mesenchymal transition-related signaling and may serve as potential targets in the treatment of renal interstitial fibrosis.

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