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Background and Purpose: Renal interstitial fibrosis is a frequent pathological manifestation of lupus nephritis (LN). tRNA halves (tiRNAs) are acquired from tRNA‐derived small non‐coding RNAs (sncRNAs) and are associated with fibrosis. Our previous study indicated enhanced tiRNA‐Gly‐GCC‐002 (tiRNA002) levels in kidneys were positively related to LN‐related fibrosis. However, the precise molecular mechanism remains unclear. Experimental Approach: The mimic and agomiR of tiRNA002 were introduced into tubular epithelial cells (TECs) and MRL/lpr mice by transfection. The levels of gene and protein expressions were quantified using real‐time quantitative polymerase chain reaction (RT‐qPCR), Western blot and immunofluorescence assays. Key Results: In TECs treated with LN serum, as well as in the kidneys of MRL/lpr mice, high levels of tiRNA002 directly influenced the epithelial‐mesenchymal transition (EMT) and extracellular matrix (ECM) deposition. Furthermore, tiRNA002 overexpression promoted EMT in TECs and accelerated renal interstitial fibrosis in MRL/lpr mice via Smad signalling. The target gene of tiRNA002, FKBP prolyl isomerase 5 (FKBP5), improved Smad signalling by interacting with phosphorylated Smad2/3. Silencing FKBP5 alleviated LN serum‐ or tiRNA002‐mimic‐induced EMT in TECs. In addition, FKBP5 overexpression reversed the tiRNA002 knockdown‐mediated reduction of EMT and ECM accumulation. Conclusions and Implications: These findings indicated that tiRNA002 is markedly increased in LN, which facilitates renal fibrosis by promoting EMT via FKBP5‐mediated Smad signalling. Therefore, targeting tiRNA002 may be an innovative approach to treat renal interstitial fibrosis in LN. [ABSTRACT FROM AUTHOR]

• Neurons express CD109 in the central nervous system. • CD109 is upregulated in the lumbar spinal cord of SOD1-G93A mice. • CD109 upregulation is mainly contributed by proliferated microglia. • CD109 inhibits TGFβ/SMAD pathway and attenuates inflammatory reactions in microglia. CD109 is a multifunctional coreceptor, whose function has been widely studied in tumor progression and metastasis. One of the reported primary roles of CD109 involves down-regulating TGFβ signaling. However, the role of CD109 in central nervous system, especially neurodegenerative disease, is barely known. Here, we examined the expression changes and cellular location of CD109 and TGFβ/SMAD pathway molecules in lumbar spinal cord of SOD1-G93A mice, and explored the role and mechanism of CD109 on LPS-treated BV2 microglia and primary microglia derived from SOD1-G93A mice. Our results showed an increased expression of CD109 and TGFβ/SMAD pathway molecules in lumbar spinal cord of SOD1-G93A mice. Further cellular localization analysis demonstrated that proliferating microglia contributed mainly to the upregulation of CD109 and TGFβ1. Moreover, CD109 intervention in vitro partially reduced inflammatory response and TGFβ/SMAD pathway activation in both LPS-treated BV2 microglia and primary SOD1-G93A microglia. Thus, CD109 was involved in pathogenesis of ALS mice, and interventions targeting on CD109 modulation could be a potential therapeutic strategy for ALS. [ABSTRACT FROM AUTHOR]

Dye degradation presents a persistent challenge in addressing water pollution. While several methods, including adsorption, biodegradation, and advanced oxidation processes, have been extensively explored, photocatalysis remains one of the most effective techniques. Conventional photocatalytic dye degradation processes often rely on expensive light sources and are time‐intensive. Herein, we synthesized a SnS catalyst by the solvated metal atom dispersion (SMAD) method, using Sn foil and sulfur powder. The catalyst exhibited remarkable performance, achieving complete degradation of methylene blue within 2 minutes under ambient room light, without the need for any external light source. Similar degradation efficiency was achieved for methyl orange. To evaluate the role of light for the degradation, control experiments were conducted in the dark using methylene blue as a model dye. Although the degradation rate was slightly reduced, the catalyst still facilitated dye degradation in the absence of light. Additionally, the catalytic performance was tested with four other dyes under natural light, all of which yielded promising results, demonstrating the versatility and effectiveness of the SnS catalyst in dye degradation. This work highlights the potential of the SnS catalyst for efficient and rapid dye degradation under both light and dark conditions, offering an energy‐efficient solution for wastewater treatment. [ABSTRACT FROM AUTHOR]

Smads and their transcription factor partners mediate the transcriptional responses of target cells to secreted ligands of the transforming growth factor-β (TGF-β) family, including those of the conserved bone morphogenetic protein (BMP) family, yet only a small number of direct target genes have been well characterized. In C. elegans, the BMP2/4 ortholog DBL-1 regulates multiple biological functions, including body size, via a canonical receptor-Smad signaling cascade. Here, we identify functional binding sites for SMA-3/Smad and its transcriptional partner SMA-9/Schnurri based on ChIP-seq peaks (identified by modEncode) and expression differences of nearby genes identified from RNA-seq analysis of corresponding mutants. We found that SMA-3 and SMA-9 have both overlapping and unique target genes. At a genome-wide scale, SMA-3/Smad acts as a transcriptional activator, whereas SMA-9/Schnurri direct targets include both activated and repressed genes. Mutations in sma-9 partially suppress the small body size phenotype of sma-3, suggesting some level of antagonism between these factors and challenging the prevailing model for Schnurri function. Functional analysis of target genes revealed a novel role in body size for genes involved in one-carbon metabolism and in the endoplasmic reticulum (ER) secretory pathway, including the disulfide reductase dpy-11 . Our findings indicate that Smads and SMA-9/Schnurri have previously unappreciated complex genetic and genomic regulatory interactions that in turn regulate the secretion of extracellular components like collagen into the cuticle to mediate body size regulation., Competing Interests: MV Works at ModOmics Ltd, no other competing interests to declare, JD, ZW, KG, JK, CR, CS No competing interests declared, (© 2024, Vora, Dietz et al.)