https://scholar.dgist.ac.kr/handle/20.500.11750/16864 2026-10-22T09:59:38Z https://scholar.dgist.ac.kr/handle/20.500.11750/60959 Title: Excessive epithelial mechanosensation drives nociceptive innervation and chronic bladder pain via the PIEZO1-SLC7A11-glutamate axis Author(s): Kim, Min Jung; Noh, Joo Hwan; Lee, Ho Young; Lee, Bohm; Park, Alexander Doh; Oh, Hyeonseo; Kim, Geun-Woo D.; Lee, Hye-Sook; Oh, Yeonsoo; Hwang, Hyeonje; Kim, Chungoo; Lee, Hyeonjong; Li, Xue; Oh, Mi Mi; Lim, Donghoon; Abraham, Soman N.; Cho, Yongcheol; Chi, Sung Wook; Choi, Hae Woong Abstract: Epithelial mechanosensation maintains tissue homeostasis by sensing mechanical stimuli. Dysregulated mechanotransduction has been implicated in chronic pain, yet the molecular link between epithelial stress and persistent sensory dysfunction remains unclear. Here, we report that the mechanosensitive ion channel PIEZO1 is markedly upregulated in bladder epithelial cells under recurrent uropathogenic E. coli infection through interleukin-6 (IL-6)-dependent signaling. PIEZO1 overexpression amplifies mechanotransductioninduced reactive oxygen species (ROS) generation, triggering a homeostatic antioxidant response via the cystine-glutamate antiporter system Xc-(SLC7A11). This protective mechanism inadvertently promotes extracellular glutamate accumulation, driving aberrant sprouting and hyperinnervation of peptidergic nociceptive C fibers into the epithelial layer. This neuroepithelial remodeling sensitizes bladder afferents and induces persistent pain-like states resembling chronic visceral pain and organ dysfunction. Our findings reveal a paradoxical role of epithelial antioxidant defense in promoting pain through the PIEZO1-SLC7A11-glutamate axis and highlight the neuroepithelial interface as a key therapeutic target for infection-induced chronic pain syndromes. 2026-07-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60570 Title: Gpr151 유전자의 5'UTR 또는 이의 변이체를 이용한 신경 손상의 치료 Author(s): 이진영; 조용철; 전예원; 이봄; 신정은 Abstract: Disclosed is a composition for treating a neurological disease caused by nerve injury, including an isolated polynucleotide of a 5′-untranslated region (5′UTR) of a Gpr151 gene or a variant thereof. Also disclosed are a novel variant polynucleotide of 5′UTR of a Gpr151 gene and a vector including the polynucleo https://scholar.dgist.ac.kr/handle/20.500.11750/60411 Title: CSDE1 Associates with TOM20 and Mitochondrial Protein-Encoding mRNAs in Sensory Neurons Author(s): Jin, Hoyong; Jang, Eunsu; Park, Eunhye; Lee, Ju Yeon; Song, Ju Hwan; Cho, Yongcheol Abstract: Mitochondrial proteostasis in neurons relies on the coordinated expression, targeting, and import of a predominantly nuclear-encoded proteome to meet high metabolic demands. Here, we identify the RNA-binding protein cold shock domain containing E1 (CSDE1) as a TOM20-associated factor linked to mitochondrial protein-encoding mRNAs in sensory neurons. CSDE1 immunoprecipitation followed by sequencing from na & iuml;ve dorsal root ganglion tissue revealed association with nuclear-encoded mitochondrial mRNAs enriched for inner membrane/matrix and oxidative phosphorylation pathways. A subset of CSDE1 localized to mitochondria and associated with the outer mitochondrial membrane import receptor TOM20 via its N-terminal region in an RNA-independent manner. In cultured sensory neurons, CSDE1 depletion reduced the mitochondrial-fraction abundance of representative nuclear-encoded electron transport chain mRNAs and decreased the abundance of selected mitochondrial proteins in the mitochondrial fraction. CSDE1 depletion reduced TMRM-positive mitochondrial puncta density along sensory neurites, without significantly increasing MitoSOX-detectable mitochondrial superoxide signals under either basal or oxidative challenge conditions. These findings identify CSDE1 as a TOM20-associated RNA-binding protein linked to mitochondrial protein-encoding transcripts in sensory neurons and support a model in which CSDE1 contributes to mitochondria-associated post-transcriptional regulation. 2026-04-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/58813 Title: TREATMENT OF NERVE DAMAGE USING 5`UTR OF GPR151 GENE OR VARIANT THEREOF Author(s): 이진영; 신정은; 전예원; 이봄; 조용철 Abstract: Disclosed is a composition for treating neurological diseases caused by nerve damage comprising an isolated polynucleotide of 5'UTR (untranslated region) of Gpr151 gene or a variant thereof. Also, disclosed are novel variant polynucleotides of 5'UTR of Gpr151 gene, and vectors comprising the polynucleotides.