LncRNA4474 inhibits renal fibrosis by regulating hepatocyte nuclear factor-1β through miR-615 modulation

Zhu, Yun; Wang, Zhenyu; Liang, Zuohui; Xu, Shuangyan; Teng, Yirong; Li, Xiaolan; Zeng, Yong

doi:10.1080/15384101.2022.2046982

Cited by 2 publications

(3 citation statements)

References 30 publications

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“…In the UUO group, the left kidney and left ureter of rats were exposed layer by layer through laparotomy; the left ureter near the renal pelvis was ligated with 3-0 silk thread, then normal saline was injected intraperitoneally 0.1 mL/day after surgery. The rats in UUO+shNC and UUO+sh-Meg3 groups were made into the ureter adjacent to the renal pelvis of shRNA-adenovirus vectors (0.1 mL/day, 1 × 10 14 virus genome copies per milliliter) and shRNA-adenovirus lncRNA Meg3 (0.1 mL/day, 1 × 10 14 virus genome copies per milliliter), respectively, after UUO [14,15]. Both shRNA and lncRNA Meg3 shRNA were synthesized by Thermo Fisher Scientific.…”

Section: Experimental Animals and Groupingmentioning

confidence: 99%

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LncRNA Meg3 Aggravates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Rats by Activating the Hedgehog Pathway

Dong,

Zhang,

et al. 2024

Discovery Medicine

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Background: The hedgehog signaling pathway exerts vital functions in regulating epithelial-to-mesenchymal transition (EMT) in renal interstitial fibrosis (RIF). It was reported that lncRNA-maternally expressed gene 3 (lncRNA Meg3) can regulate hepatic fibrosis by regulating the expression of smoothened (Smo) in the hedgehog signaling pathway. However, the specific role of lncRNA Meg3 in renal fibrosis resulting from unilateral ureteral obstruction (UUO) by regulating the hedgehog signaling pathway has not been reported. Hence, this research aimed to expound the effects of lncRNA Meg3 on renal fibrosis induced by UUO in rats via the hedgehog pathway. Methods: Peripheral blood was collected from patients with chronic kidney disease (CKD, CKD group) and healthy volunteers (Normal group) at the same period. In addition, 6-week-old male Sprague-Dawley (SD) rats were divided to Sham, UUO, UUO+shRNA Negative control (shNC), and UUO+sh-Meg3 groups, and their kidney tissues and serum were gathered. Next, quantitative real-time polymerase chain reaction (qRT-PCR) was employed for detecting the lncRNA Meg3 expression level in the serum of patients and renal tissue of rats; kits for testing levels of blood urea nitrogen (BUN), creatinine (Cr), hydroxyproline (HYP), and 24-hour urine protein (24-up) in rats of each group; hematoxylin and eosin (HE) staining and Masson staining for observing kidney tissue and renal fibrosis level in rats; western blot for measuring levels of collagen type III (Col III), α-Smooth muscle actin (α-SMA), fibronectin, E-cadherin, sonic hedgehog (Shh), patched (Ptch) protein, smoothened (Smo) protein and glioma-associated oncogene homolog 1 (Gli1) protein expression. Results: LncRNA Meg3 was highly expressed in CKD patients and UUO rats (p < 0.01). In contrast to the UUO+shNC group, knocking down lncRNA Meg3 improved renal injury, relieved pathological renal lesions, and reduced kidney fibrosis and related protein levels. It inhibited the hedgehog pathway in kidney tissues of UUO rats (p < 0.05 and p < 0.01). Conclusions: LncRNA Meg3 can aggravate UUO-induced rat renal fibrosis by activating the hedgehog pathway.

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Section: Experimental Animals and Groupingmentioning

confidence: 99%

“…Glyceraldehyde-3phosphate dehydrogenase (GAPDH) was used as the internal control of lncRNA expression. The relative transcription level of target genes was calculated through the relative quantitative method (2 −∆∆Ct method) [14]. Besides, all samples were provided with 3 wells, and each test was repeated 3 times.…”

Section: Qrt-pcrmentioning

confidence: 99%

LncRNA Meg3 Aggravates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Rats by Activating the Hedgehog Pathway

Dong,

Zhang,

et al. 2024

Discovery Medicine

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“…lncRNA4474 overexpression increased the expression of HNF-1β by reducing miR-615 expression ( Fig. 1F ), and inactivated the Wnt signaling pathway ( 74 ).…”

Section: Dysregulated Lncrnas In Liver and Kidney Fibrosismentioning

confidence: 99%

Long non-coding RNAs: key regulators of liver and kidney fibrogenesis

Han

Kang

et al. 2023

BMB Rep

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Fibrosis is a pathological condition that is characterized by an abnormal buildup of extracellular matrix (ECM) components, such as collagen, in tissues. This condition affects various organs of the body, including the liver and kidney. Early diagnosis and treatment of fibrosis are crucial, as it is a progressive and irreversible process in both organs. While there are certain similarities in the fibrosis process between the liver and kidney, there are also significant differences that must be identified to determine molecular diagnostic markers and potential therapeutic targets. Long non-coding RNAs (lncRNAs), a class of RNA molecules that do not code for proteins, are increasingly recognized as playing significant roles in gene expression regulation. Emerging evidence suggests that specific lncRNAs are involved in fibrosis development and progression by modulating signaling pathways, such as the TGF-β/Smad pathway and the β-catenin pathway. Thus, identifying the precise lncRNAs involved in fibrosis could lead to novel therapeutic approaches for fibrotic diseases. In this review, we summarize lncRNAs related to fibrosis in the liver and kidney, and propose their potential as therapeutic targets based on their functions.

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LncRNA4474 inhibits renal fibrosis by regulating hepatocyte nuclear factor-1β through miR-615 modulation

Cited by 2 publications

References 30 publications

LncRNA Meg3 Aggravates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Rats by Activating the Hedgehog Pathway

LncRNA Meg3 Aggravates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Rats by Activating the Hedgehog Pathway

Long non-coding RNAs: key regulators of liver and kidney fibrogenesis

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