Metabolic regulator LKB1 controls adipose tissue ILC2 PD-1 expression and mitochondrial homeostasis to prevent insulin resistance.

Adipose tissue group 2 innate lymphoid cells (ILC2s) help maintain metabolic homeostasis by sustaining type 2 immunity and promoting adipose beiging. Although impairment of the ILC2 compartment contributes to obesity-associated insulin resistance, the underlying mechanisms have not been elucidated. Here, we found that ILC2s in obese mice and humans exhibited impaired liver kinase B1 (LKB1) activation. Genetic ablation of LKB1 disrupted ILC2 mitochondrial metabolism and suppressed ILC2 responses, resulting in exacerbated insulin resistance. Mechanistically, LKB1 deficiency induced aberrant PD-1 expression through activation of NFAT, which in turn enhanced mitophagy by suppressing Bcl-xL expression. Blockade of PD-1 restored the normal functions of ILC2s and reversed obesity-induced insulin resistance in mice. Collectively, these data present the LKB1-PD-1 axis as a promising therapeutic target for the treatment of metabolic disease.

SUMO-specific protease 1 regulates germinal center B cell response through deSUMOylation of PAX5.

Humoral immunity depends on the germinal center (GC) reaction where B cells are tightly controlled for class-switch recombination and somatic hypermutation and finally generated into plasma and memory B cells. However, how protein SUMOylation regulates the process of the GC reaction remains largely unknown. Here, we show that the expression of SUMO-specific protease 1 (SENP1) is up-regulated in GC B cells. Selective ablation of SENP1 in GC B cells results in impaired GC dark and light zone organization and reduced IgG1-switched GC B cells, leading to diminished production of class-switched antibodies with high-affinity in response to a TD antigen challenge. Mechanistically, SENP1 directly binds to Paired box protein 5 (PAX5) to mediate PAX5 deSUMOylation, sustaining PAX5 protein stability to promote the transcription of activation-induced cytidine deaminase. In summary, our study uncovers SUMOylation as an important posttranslational mechanism regulating GC B cell response.

Up-regulation of BTN3A1 on CD14+ cells promotes Vγ9Vδ2 T cell activation in psoriasis.

Vγ9Vδ2 T cells play an important role in the development and progression of psoriasis vulgaris (PV), but how they promote skin inflammation and the molecular mechanisms underlying Vγ9Vδ2 T cell dysfunction are poorly understood. Here, we show that circulating Vγ9Vδ2 T cells are decreased and exhibit enhanced proliferation and increased production of IFN-γ and TNF-α in PV patients. Monocytes from PV patients express higher levels of the phosphoantigen sensor butyrophilin 3A1 (BTN3A1) than monocytes from healthy controls. Blockade of BTN3A1 suppresses Vγ9Vδ2 T cell activation and abolishes the difference in Vγ9Vδ2 T cell activation between PV patients and healthy controls. The CD14+ cells in PV skin lesions highly express BTN3A1 and juxtapose to Vδ2 T cells. In addition, IFN-γ induces the up-regulation of BTN3A1 on monocytes. Collectively, our results demonstrate a crucial role of BTN3A1 on monocytes in regulating Vγ9Vδ2 T cell activation and highlight BTN3A1 as a potential therapeutic target for psoriasis.

Serum Phosphorus Might Be a Predictor of Kidney Disease Progression in IgA Nephropathy.

INTRODUCTION: High serum phosphorus level has been reported to be a risk factor for disease progression in patients with chronic kidney disease, whereas, its role in IgA nephropathy (IgAN) still remains uncertain. This study aimed to investigate the association between serum phosphorus and progression of IgAN. METHODS: A total of 247 patients diagnosed with IgAN from 2016.11 to 2019.12 at the First Affiliated Hospital of Xi'an Jiaotong University were retrospectively enrolled in this study. The association between serum phosphorus and kidney disease progression events, defined as 30% estimated glomerular filtration rate (eGFR) decline or kidney failure, was evaluated using Cox models. RESULTS: Serum phosphorus was an independent risk factor for poor renal outcome after adjusting for age, gender, urine protein, MAP, eGFR, hemoglobin, Oxford S and T scores (HR, 2.586; 95% CI, 1.238-5.400, p = 0.011). The addition of serum phosphorus to the reference model containing clinical and pathological variables significantly improved the risk prediction of IgAN progression (C statistic, 0.836; 95% CI, 0.783-0.889) as compared with the reference model (C statistic, 0.821; 95% CI, 0.756-0.886). The ability of serum phosphorus level to predict progression was much stronger in IgAN patients without use of immunosuppression (HR 5.173; 95% CI, 1.791-14.944; p = 0.002). CONCLUSION: Higher serum phosphorus levels were independently associated with kidney disease progression in patients with IgAN, especially in those without immunosuppression. The addition of serum phosphorus to clinical and pathological data at the time of biopsy significantly improved risk prediction of IgAN progression.

Are USPD patients suitable for incremental peritoneal dialysis: Yes or no?

BACKGROUND: Incremental peritoneal dialysis (IPD) is the practice of initiating PD exchange less than 4 times a day in consideration of residual renal function (RRF). This study determined whether IPD could be used for urgent-start peritoneal dialysis (USPD) patients when starting dialysis, and when compared to full-dose PD, could IPD affect the RRF in USPD patients. MATERIALS AND METHODS: 169 USPD patients with eGFR between 4 and 6 mL/min/1.73m2 were retrospectively analyzed. The duration of follow-up was 1 year. Patients were divided into an incremental PD (i-PD) group (dialysis dose ≤ 6,000 mL) and a full-dose PD (f-PD) group (dialysis dose ≥ 8,000 mL). The demographics, clinical indices, peritoneal transport function, dialysis adequacy, and complications of peritoneal dialysis were compared between both groups. RESULTS: (1) 111 patients (average age 45.01 ± 12.84 years) were included in the i-PD group and 58 patients (average age 43.5 ± 15.62 years) in the f-PD group. The demographics and clinical indices of both groups before PD were similar (p < 0.05). (2) During the follow-up period, the dialysis dose in the f-PD group exceeded that of the i-PD group (p < 0.05). The dialysis adequacy of both groups was as expected. (3) During the follow-up period, peritoneal transport function, the RRF, the blood pressure control, correction of anemia, and correction of calcium and phosphorus abnormalities were similar in both groups. (4) The peritoneal dialysis-related infection, mechanical complications, and technical survival rate were similar between groups. CONCLUSION: Incremental PD did not cause a rapid decline of RRF in USPD patients. The dialysis effect and complications from it, were similar to full-dose peritoneal dialysis. Thus, USPD patients can be treated by IPD.

The effects of peritoneal dialysis on QT interval in ESRD patients.

BACKGROUND: Patients with chronic kidney disease (CKD) are at a high risk of fatal arrhythmias. The extended corrected QT (QTc) interval is a hallmark of ventricular arrhythmias and sudden cardiac death. Previous studies have shown that QT interval and QTc are prolonged with the decline in renal function. However, there were no available results for patients with peritoneal dialysis (PD). In this study, we examined changes in QT interval and QTc in patients with end-stage renal disease (ESRD) who underwent peritoneal dialysis. METHODS: A total of 66 ESRD patients who received PD, including 50 males and 16 females, with an average age of 43.56 ± 15.15 years, were enrolled. The follow-up lasted 1 year. The demographics and the etiology of patients were recorded. QTc and clinical/biochemical indexes before dialysis and at 6 and 12 months were determined and analyzed. Dialysis adequacy and peritoneal transport function were assessed in each patient. Analysis of variance (ANOVA), least significant difference (LSD) or Tamhane's T2, Paired T-test, Chi-square test, multiple linear regression analysis, and Pearson correlation coefficient were used to analyze the data. P < 0.05 was considered as statistically significant. RESULTS: With reference to etiology, 37 patients (56.06%) had chronic nephritis, and 11 (16.67%) had diabetic nephropathy. Most of the peritoneal transport functions were low average transport (25, 37.88%), while the least were high transport (2, 3.03%).During the follow-up period, all patients had adequate peritoneal dialysis. Compared with a baseline before dialysis, anemia, low albumin, blood pressure, blood urea nitrogen, creatinine, uric acid, potassium, calcium, phosphorus, and parathyroid hormone improved after 6 and 12 months, while the residual renal function gradually decreased during the follow-up. The mean QTc of all patients was stable during the follow-up period. According to gender, the QTc in males and female patients were similar. Before PD, diastolic blood pressure, calcium concentration, and hemoglobin level were negatively correlated with QTc in end-stage renal disease patients; After PD, the observed clinical indexes were no longer relevant to QTc. CONCLUSION: Unlike hemodialysis-induced QTc prolongation, PD did not increase the patient's QT interval and QTc interval, which suggested that myocardial electrical activity might be more stable in patients with adequate peritoneal dialysis.

MZB1 promotes the secretion of J-chain-containing dimeric IgA and is critical for the suppression of gut inflammation.

IgA is the most abundantly produced antibody in the body and plays a crucial role in gut homeostasis and mucosal immunity. IgA forms a dimer that covalently associates with the joining (J) chain, which is essential for IgA transport into the mucosa. Here, we demonstrate that the marginal zone B and B-1 cell-specific protein (MZB1) interacts with IgA through the α-heavy-chain tailpiece dependent on the penultimate cysteine residue and prevents the intracellular degradation of α-light-chain complexes. Moreover, MZB1 promotes J-chain binding to IgA and the secretion of dimeric IgA. MZB1-deficient mice are impaired in secreting large amounts of IgA into the gut in response to acute inflammation and develop severe colitis. Oral administration of a monoclonal IgA significantly ameliorated the colitis, accompanied by normalization of the gut microbiota composition. The present study identifies a molecular chaperone that promotes J-chain binding to IgA and reveals an important mechanism that controls the quantity, quality, and function of IgA.

Distinct roles of BCNP1 in B-cell development and activation.

B-cell novel protein 1 (BCNP1) has recently been identified as a new B-cell receptor (BCR) signaling molecule but its physiological function remains unknown. Here, we demonstrate that mice deficient in BCNP1 exhibit impaired B-cell maturation and a reduction of B-1a cells. BCNP1-deficient spleen B cells show enhanced survival, proliferation and Ca2+ influx in response to BCR cross-linking as compared with wild-type spleen B cells. Consistently, mutant B cells show elevated phosphorylation of SYK, B-cell linker protein (BLNK) and PLCγ2 upon BCR cross-linking. In vivo, BCNP1-deficient mice exhibit enhanced humoral immune responses to T-independent and T-dependent antigens. Moreover, aged mutant mice contain elevated levels of serum IgM and IgG3 antibodies and exhibit polyclonal and monoclonal B-cell expansion in lymphoid organs. These results reveal distinct roles for BCNP1 in B-cell development, activation and homeostasis.

PTPN13 acts as a tumor suppressor in clear cell renal cell carcinoma by inactivating Akt signaling.

Protein tyrosine phosphatase, nonreceptor type 13 (PTPN13), has emerged as a critical cancer-related gene that is implicated in a wide range of cancer types. However, the role of PTPN13 in clear cell renal cell carcinoma (ccRCC) is poorly understood. In the present study, we aimed to evaluate whether PTPN13 participates in the progression of ccRCC. Decreased expression of PTPN13 was found in ccRCC tissues, which predicted a shorter survival rate in ccRCC patients. PTPN13 expression was also lower in ccRCC cell lines, and the upregulation of PTPN13 repressed the proliferation, colony formation and invasion, but enhanced the apoptosis of ccRCC cells. In contrast, the silencing of PTPN13 produced the opposite effects. Further data showed that PTPN13 overexpression decreased the phosphorylation of Akt, while PTPN13 silencing increased the phosphorylation of Akt. Treatment with Akt inhibitor markedly abrogated the PTPN13 silencing-evoked oncogenic effect in ccRCC cells. Xenograft tumor experiments revealed that overexpression of PTPN13 remarkably restricted the tumor formation and growth of ccRCC cells in vivo associated with inactivation of Akt. In conclusion, our data demonstrated that overexpression of PTPN13 restricts the proliferation and invasion of ccRCC cells through inactivation of Akt. Our study suggests a tumor suppressive function of PTPN13 in ccRCC and highlights the potential role of PTPN13 in the progression of ccRCC.

Circular RNAs Interaction with MiRNAs: Emerging Roles in Breast Cancer.

Despite significant advances in cancer therapy strategies, breast cancer is one of the most common and lethal malignancies worldwide. Characterization of a new class of RNAs using next-generation sequencing opened new doors toward uncovering etiopathogenesis mechanisms of breast cancer as well as prognostic and diagnostic biomarkers. Circular RNAs (circRNAs) are a novel class of RNA with covalently closed and highly stable structures generated primarily from the back-splicing of precursor mRNAs. Although circRNAs exert their function through various mechanisms, acting as a sponge for miRNAs is their primary mechanism of function. Furthermore, growing evidence has shown that aberrant expression of circRNAs is involved in the various hallmarks of cancers. This paper reviews the biogenesis, characteristics, and mechanism of functions of circRNAs and their deregulation in various cancers. Finally, we focused on the circRNAs roles as a sponge for miRNAs in the development, metastasis, angiogenesis, drug resistance, apoptosis, and immune responses of breast cancer.

Using overlapping low-profile visualized intraluminal support stent-assisted coil embolization for treating blood blister-like aneurysms of the internal carotid artery.

Blood blister-like aneurysm (BBA) of the internal carotid artery (ICA) is highly challenging to treat owing to its variable morphology and tendency for rupture and regrowth. In this study, we attempted to discuss the key techniques for overlapping low-profile visualized intraluminal support (LVIS) stent-assisted coil embolization, which is used for treating BBAs in our center. Clinical characteristics, endovascular treatment details, outcomes, and follow-up results of 13 patients with BBA treated at our center were retrospectively evaluated in this study. Overlapping LVIS stent-assisted coil embolization was successfully performed in all 13 patients of ruptured BBAs located in the ICAs. Recurrence of aneurysm was observed in 4 cases (30.8%) during the angiographic follow-up; in 2 of these cases, spontaneous healing was observed after discontinuation of antiplatelet therapy. Further, 2 patients with recurrence underwent endovascular treatment with complete obliteration of the aneurysm in one and occlusion of the parent artery after Onyx embolization and stent placement in the other. The overall obliteration rate of the BBAs was 92.3% (12/13). One patient (7.7%) developed intraoperative rupture of the aneurysm with coils protruding outside; however, no severe hemorrhage or neurological dysfunction occurred owing to timely embolization. Overlapping LVIS stent-assisted coil embolization is effective for management of BBA of the ICA. Appropriate adjustment in antiplatelet therapy may improve healing in recurrent cases.

LncRNA MIAT enhances systemic lupus erythematosus by upregulating CFHR5 expression via miR-222 degradation.

Systemic lupus erythematosus (SLE), a complex polygenic autoimmune disease, is associated with increased complement activation. Complement factor H related protein 5 (CFHR5) may contribute to dysfunctional complement activation, thus predisposing to SLE. The expression levels of anti-dsDNA, C3 and CFHR5 in blood samples from 50 SLE patients and 50 healthy individuals were evaluated, and also their expression levels were measured in an MRL/lpr mouse model and control MRL/MPJ mice. The results showed that CFHR5 expression increased in SLE patients together with the increase of anti-dsDNA in comparison with the healthy control. Furthermore, CFHR5 expression was inversely correlated with C3, down-regulation of which was associated with worse SLE. Previous studies indicated that long noncoding RNA (lncRNA) regulates mRNA synthesis via microRNA (miRNA) inhibition. The present bioinformatics analysis revealed that the target miRNA (miR-222) was combined with both lncRNA MIAT and mRNA CFHR5. H&E staining of the kidney tissues of the MRL/lpr mice revealed that lncRNA MIAT, as a competitive inhibitor of miR-222, enhanced SLE by upregulating CFHR5 expression through the degradation of miR-222 in vivo. Thus, our study revealed for the first time the role of lncRNA MIAT in regulating CFHR5 expression in SLE in vivo and provided new insights into the role of lncRNA in regulation and complement function of SLE pathogenesis.

MiR-325-3p inhibits renal inflammation and fibrosis by targeting CCL19 in diabetic nephropathy.

Diabetic nephropathy (DN), a common cardiovascular disease, has been a global health threat. MicroRNAs (miRNAs) have been proposed to frequently participate in the occurrence and development of DN, however, the role of miR-325-3p in DN remains uncharacterized. Our research aimed to explore the function and mechanism of miR-325-3p in DN. Bioinformatics analysis (Targetscan, http://www.targetscan.org) and a wide range of experiments including RT-qPCR, CCK-8 assay, western blot, luciferase reporter assay, RNA immunoprecipitation (RIP) assays, urine protein and blood glucose assays, histology analysis and morphometric analysis were used to explore the function and mechanism of miR-325-3p and C-C motif chemokine ligand 19 (CCL19). CCL19 could facilitate the progression of DN by inhibiting cell viability and promoting inflammation and fibrosis in HK-2 and HMC cells. In addition, CCL19 was confirmed to be targeted and negatively regulated by miR-325-3p. Rescue assays validated that the impacts of miR-325-3p mimics on the viability, inflammation and fibrosis of HK-2 and HMC cells were recovered by CCL19 overexpression. To sum up, miR-325-3p inhibits renal inflammation and fibrosis by targeting CCL19 in a DN cell model and mice model, implying miR-325-3p as a possible therapeutic target for DN treatment.

Inhibitor of growth 4 inhibits cell proliferation, migration, and induces apoptosis of renal cell carcinoma cells.

The inhibitor of growth 4 (ING4) is known as a tumor suppressor. The expressions of ING4 were markedly reduced in human renal clear cell carcinoma (ccRCC) tissues. However, the role of ING4 in renal cell carcinoma (RCC) remains unknown. The aim of the current study was to detect the ING4 expression level and its potential role in human RCC cell lines. Our results showed that ING4 was lowly expressed in human RCC cell lines compared with that in proximal tubular cell line. Ectopic overexpression of ING4 inhibited the proliferation, migration, and invasion properties, and as well as prevented epithelial-mesenchymal transition (EMT) phenotype of RCC cells. In addition, ING4 overexpression induced cell apoptosis and autophagy in RCC cells. Furthermore, ING4 overexpression suppressed the activation of PI3K/Akt pathway in RCC cells. The activator of PI3K/Akt, insulin-like growth factor 1, abolished the effects of ING4 on RCC cells. These findings indicated that ING4 presented anticancer activity in RCC cells. The effects of ING4 on RCC cells were mediated by regulating the PI3K/Akt pathway. These findings suggested that ING4 could be used for gene therapy of RCC.

Expression of Vsig4 attenuates macrophage-mediated hepatic inflammation and fibrosis in high fat diet (HFD)-induced mice.

The innate immune response contributes to hepatic steatosis and nonalcoholic fatty liver disease (NAFLD). However, the pathogenic mechanism of NAFLD is still poorly understood. The costimulatory molecule V-set and immunoglobulin domain-containing protein-4 (Vsig4), which is exclusively expressed on macrophages, shows significant role in regulating macrophage-mediated inflammation. Here, we attempted to explore if Vsig4 expression was involved in high fat diet (HFD)-induced NAFLD. The results indicated that Vsig4 expression was markedly down-regulated in fatty livers of NAFLD patients and obese mice. Vsig4 knockout accelerated HFD-induced metabolic dysfunction. In addition, the loss of Vsig4 significantly promoted insulin resistance and lipid deposition in liver samples of HFD-challenged mice. Furthermore, HFD-induced inflammation was apparently accelerated in Vsig4 knockout mice by further activating nuclear factor-κB (NF-κB) signaling pathway. Also, Vsig4 deficient mice exhibited greater collagen accumulation in hepatic samples in HFD-challenged mice compared to the WT mice, which was through promoting transforming growth factor-ß1 (TGFß1) signaling. Importantly, we found that lipopolysaccharide (LPS)- or TGFß1-stimulated inflammation and fibrosis in primary hepatocytes and hepatic stellate cells, respectively, were markedly exacerbated by co-culture with condition medium from bone marrow-derived macrophages (BMDMs) with Vsig4 deficiency. Finally, transplantation of bone marrow cells from control mice to Vsig4-knockout mice restored the severity of steatosis, inflammation and fibrosis after HFD feeding. Therefore, loss of Vsig4 accelerated the severity of lipid deposition, fibrosis and the inflammatory response. Vsig4 could be a therapeutic target for NAFLD treatment.

Opposing roles of IgM and IgD in BCR-induced B-cell survival.

The B-cell receptor (BCR) transmits a tonic survival signal in the absence of antigen stimulation and an antigen-triggered survival signal. Mature B cells express two types of BCR, IgM and IgD, but it remains unclear how B-cell survival is differentially regulated by these two receptors. We found that, whereas cross-linking IgM on spleen B cells greatly enhanced their survival, cross-linking IgD did not enhance, but rather decreased, their survival. Consistently, cross-linking both IgM and IgD only moderately enhanced B-cell survival, suggesting that IgM and IgD play opposing roles in B-cell survival induced by BCR stimulation. Based on these and additional experimental results, we present a mathematical model integrating IgM- and IgD-mediated survival signals. Our model shows that IgD can transmit a tonic survival signal in the absence of antigen stimulation but cross-linking IgD not only does not generate a survival signal but also disrupts its tonic signal, resulting in inhibition of B-cell survival. These results suggest that IgD attenuates BCR-induced survival in mature B cells, presumably to restrain B-cell response to weak and/or self-antigens and prevent nonspecific B-cell activation and autoimmunity.

BMSCs and miR-124a ameliorated diabetic nephropathy via inhibiting notch signalling pathway.

BMSCs are important in replacement therapy of diabetic nephropathy (DN). MiR-124a exerts effect on the differentiation capability of pancreatic progenitor cells. The objective of this study was to explore the molecular mechanisms, the functions of miR-124a and bone marrow mesenchymal stem cells (BMSCs) in the treatment of DN. Characterizations of BMSCs were identified using the inverted microscope and flow cytometer. The differentiations of BMSCs were analysed by immunofluorescence assay and DTZ staining. The expression levels of islet cell-specific transcription factors, apoptosis-related genes, podocytes-related genes and Notch signalling components were detected using quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot assays. The production of insulin secretion was detected by adopting radioimmunoassay. Cell proliferation and apoptosis abilities were detected by CCK-8, flow cytometry and TUNEL assays. We found that BMSCs was induced into islet-like cells and that miR-124a could promote the BMSCs to differentiate into islet-like cells. BMSCs in combination with miR-124a regulated islet cell-specific transcription factors, apoptosis-related genes, podocytes-related genes as well as the activity of Notch signalling pathway. However, BMSCs in combination with miR-124a relieved renal lesion caused by DN and decreased podocyte apoptosis caused by HG. The protective effect of BMSCs in combination with miR-124a was closely related to the inactivation of Notch signalling pathway. MSCs in combination with miR-124a protected kidney tissue from impairment and inhibited nephrocyte apoptosis in DN.

Combination with miR-124a improves the protective action of BMSCs in rescuing injured rat podocytes from abnormal apoptosis and autophagy.

This in vitro study was performed to identify the role of miR-124a in bone marrow stromal stem cells (BMSCs) therapy for H2 O2 -induced rat podocyte injury, and determine whether combination treatment with miR-124a could improve the protective effect of BMSCs. Cell viability of podocytes was detected by CCK-8 assay. Detection of ROS level, apoptotic rate, and autophagy rate was carried out using flow cytometry assays. Oxidative stress parameters were analyzed using the ELISA assays. MiR-124a and mRNA levels were determined using real-time PCR. Protein expression was detected using Western blotting. Our study revealed a pivotal role of miR-124a in the protective action of BMSCs on podocyte injury driven by oxidative stress. BMSCs could rescue injured podocytes from aberrant apoptosis and autophagy by regulating cleaved caspase-3, Bax, Bcl-2, LC3-II/I, and p62. Suppression of the PI3 K/Akt/mTOR signaling pathway is likely one of the main mechanisms underlying the protective action of BMSCs transfected with miR-124a. Our study revealed that miR-124a further improves the protective effect of BMSCs in injured podocytes. Thus, the combination of BMSCs and microRNAs could be a beneficial treatment for renal diseases in the near future.

Protection of tubular epithelial cells during renal injury via post-transcriptional control of BMP7.

Severe injury of renal tubular epithelial cells may cause acute renal failure, the progression of which results in renal fibrosis, and obstructive nephropathy. Transforming growth factor ß 1 and bone morphogenic protein 7 (BMP7) play contradicting roles in and coordinate the process of epithelial-to-mesenchymal transition of renal tubular epithelial cells, but the molecular regulation of BMP7 remains ill-defined. Here, we addressed this question. We found that after induction of unilateral ureteral obstruction (UUO) in mice, the increases in BMP7 mRNA were much more pronounced than BMP7 protein in kidney, suggesting the presence of post-transcriptional control of BMP7. Moreover, significant increases in a BMP7-targeting microRNA, miR-384-5p, were detected in the mouse kidney post UUO. Overexpression of miR-384-5p significantly decreased BMP7 protein, while depletion of miR-384-5p significantly increased BMP7 protein in renal epithelial cells. Bioinformatics study showed that miR-384-5p appeared to suppress BMP7 protein translation, through its direct binding to the 3'-UTR of BMP7 mRNA. Furthermore, suppression of miR-384-5p in vivo attenuated severity of renal injury by UUO. Together, our study sheds light on miR-384-5p as a crucial factor that regulates the fibrosis-related pathogenesis after renal injury, and points to miR-384-5p as a promising innovative therapeutic target for prevention of renal fibrosis.