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  <title>Repository Collection: null</title>
  <link rel="alternate" href="https://scholar.dgist.ac.kr/handle/20.500.11750/319" />
  <subtitle />
  <id>https://scholar.dgist.ac.kr/handle/20.500.11750/319</id>
  <updated>2026-10-03T20:07:51Z</updated>
  <dc:date>2026-10-03T20:07:51Z</dc:date>
  <entry>
    <title>A novel role of erythropoietin in skin pigmentation through melanin production</title>
    <link rel="alternate" href="https://scholar.dgist.ac.kr/handle/20.500.11750/60855" />
    <author>
      <name>Han, Min Ae</name>
    </author>
    <author>
      <name>Kang, Eunho</name>
    </author>
    <author>
      <name>Kwon, Oh-Hoon</name>
    </author>
    <author>
      <name>Kim, So Yeon</name>
    </author>
    <author>
      <name>Moon, Cheil</name>
    </author>
    <author>
      <name>Lee, Chang-Hun</name>
    </author>
    <id>https://scholar.dgist.ac.kr/handle/20.500.11750/60855</id>
    <updated>2026-09-21T09:10:16Z</updated>
    <published>2026-03-31T15:00:00Z</published>
    <summary type="text">Title: A novel role of erythropoietin in skin pigmentation through melanin production
Author(s): Han, Min Ae; Kang, Eunho; Kwon, Oh-Hoon; Kim, So Yeon; Moon, Cheil; Lee, Chang-Hun
Abstract: Melanin protects the skin from UV radiation and oxidative stress. Its synthesis in melanocytes is regulated by alpha-MSH and the Melanocortin 1 Receptor signaling pathway. The erythropoietin receptor (EPOR) is expressed in melanocytes; however, its function is unknown. EPOR is a receptor for erythropoietin (EPO), which promotes hematopoiesis and protection from hypoxic stress. We hypothesized that EPOR is involved in pigment regulation. Mouse skin tissue models, cultured melanocytes, and human-derived artificial skin models were treated with recombinant human EPO (rhEPO) and/or EPO-derived peptides, and examined changes in pigmentation and cell signaling pathways. rhEPO significantly increased pigmentation, induced ERK and AKT phosphorylation, and increased tyrosinase expression in mouse melanocytes. Some EPO-derived peptides increased pigmentation in an artificial human skin model. Our results indicate that EPOR activation acts as a regulator of melanin synthesis and suggest that EPOR agonists have potential for the treatment of pigment-related diseases as well as cosmetic applications.</summary>
    <dc:date>2026-03-31T15:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Glial pathology networks reveal early olfactory vulnerability in post mortem human Alzheimer&amp;apos;s disease</title>
    <link rel="alternate" href="https://scholar.dgist.ac.kr/handle/20.500.11750/60845" />
    <author>
      <name>Jung, Da Hae</name>
    </author>
    <author>
      <name>Park, Eunji</name>
    </author>
    <author>
      <name>Ju, Hyeon Chang</name>
    </author>
    <author>
      <name>Moon, Cheil</name>
    </author>
    <author>
      <name>Jahanshahi, Ali</name>
    </author>
    <id>https://scholar.dgist.ac.kr/handle/20.500.11750/60845</id>
    <updated>2026-09-11T18:01:11Z</updated>
    <published>2026-03-31T15:00:00Z</published>
    <summary type="text">Title: Glial pathology networks reveal early olfactory vulnerability in post mortem human Alzheimer&amp;apos;s disease
Author(s): Jung, Da Hae; Park, Eunji; Ju, Hyeon Chang; Moon, Cheil; Jahanshahi, Ali
Abstract: INTRODUCTION: The olfactory system is an early target in Alzheimer's disease (AD), yet regional glial pathology interactions remain poorly defined. We examined how glial activation and pathological burden differ between the olfactory cortex (OC) and olfactory bulb (OB) across disease stages. METHODS: Post mortem OC and OB samples from cognitively normal (CN), mild cognitive impairment, and AD cases were analyzed using immunohistochemistry and immunofluorescence for amyloid beta (A beta), phosphorylated tau (pTau), Iba1 (microglia), GFAP (astrocyte), and apolipoprotein E (apoE). RESULTS: Both regions showed stage-dependent increases in A beta and pTau, with regionally distinct glial responses. ApoE signal varied with clinical stage rather than genotype. Co-expression analyses revealed astrocyte-linked networks in the OC and microglia-linked relationships in the OB. DISCUSSION: Findings demonstrate spatially heterogenous glial pathology architectures in the human olfactory system, supporting its role as an early and regionally diverse site of AD vulnerability.</summary>
    <dc:date>2026-03-31T15:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Expression and purification of the ectodomain of erythropoietin receptor fused to mCitrine or mTFP1 fluorescent protein in Escherichia coli</title>
    <link rel="alternate" href="https://scholar.dgist.ac.kr/handle/20.500.11750/60516" />
    <author>
      <name>강은호</name>
    </author>
    <author>
      <name>Ashim Janbolat</name>
    </author>
    <author>
      <name>Ji, Sangho</name>
    </author>
    <author>
      <name>Han, Min Ae</name>
    </author>
    <author>
      <name>Yu, Wookyung</name>
    </author>
    <author>
      <name>Kim, Sung Jae</name>
    </author>
    <author>
      <name>Hong, Eunmi</name>
    </author>
    <author>
      <name>Moon, Cheil</name>
    </author>
    <author>
      <name>Lee, Chang-Hun</name>
    </author>
    <id>https://scholar.dgist.ac.kr/handle/20.500.11750/60516</id>
    <updated>2026-07-27T01:10:17Z</updated>
    <published>2026-06-30T15:00:00Z</published>
    <summary type="text">Title: Expression and purification of the ectodomain of erythropoietin receptor fused to mCitrine or mTFP1 fluorescent protein in Escherichia coli
Author(s): 강은호; Ashim Janbolat; Ji, Sangho; Han, Min Ae; Yu, Wookyung; Kim, Sung Jae; Hong, Eunmi; Moon, Cheil; Lee, Chang-Hun
Abstract: The erythropoietin receptor (EPOR) is a single-pass transmembrane protein that homo-dimerizes upon binding with its renal ligand erythropoietin (EPO) to trigger downstream signaling. Its extracellular ectodomain mediates ligand binding. Therefore, a fusion protein of the EPOR ectodomain can be useful for various in vitro assays, such as a binding assay with an EPO-like peptide, if overexpressed in Escherichia coli (E.coli). In this study, we hypothesized that fusion proteins of the EPOR ectodomain with mCitrine or mTFP1, expressed in bacteria, could enable in vitro Fo &amp; uml;rster resonance energy transfer experiments. Two fusion proteins, EPOR-mCitrine and EPORmTFP1, were overexpressed in E. coli but obtained as inclusion bodies. Urea solubilization and stepwise dialysis yielded soluble fusion proteins. Circular dichroism spectroscopy revealed that EPOR-mCitrine had greater secondary structure content than EPOR-mTFP1. When combined with recombinant human EPO, the hydrodynamic radius of EPOR-mCitrine changed, as measured using dynamic light scattering, confirming binding. This interaction was further validated using isothermal titration calorimetry. We propose that bacterially produced EPOR-mCitrine is a useful in vitro tool for measuring EPO binding.</summary>
    <dc:date>2026-06-30T15:00:00Z</dc:date>
  </entry>
  <entry>
    <title>MLPH-mediated activation of dermal papilla IGF-1 signaling drives human hair shaft elongation and anagen induction</title>
    <link rel="alternate" href="https://scholar.dgist.ac.kr/handle/20.500.11750/60353" />
    <author>
      <name>Kwack, Mi Hee</name>
    </author>
    <author>
      <name>Kang, Eunho</name>
    </author>
    <author>
      <name>Kim, Jewoo</name>
    </author>
    <author>
      <name>Ji, Youngheum</name>
    </author>
    <author>
      <name>Ju, Hyeonchang</name>
    </author>
    <author>
      <name>Lee, Chang-Hun</name>
    </author>
    <author>
      <name>Sung, Young Kwan</name>
    </author>
    <author>
      <name>Kim, So Yeon</name>
    </author>
    <author>
      <name>Moon, Cheil</name>
    </author>
    <id>https://scholar.dgist.ac.kr/handle/20.500.11750/60353</id>
    <updated>2026-05-11T09:10:14Z</updated>
    <published>2026-02-28T15:00:00Z</published>
    <summary type="text">Title: MLPH-mediated activation of dermal papilla IGF-1 signaling drives human hair shaft elongation and anagen induction
Author(s): Kwack, Mi Hee; Kang, Eunho; Kim, Jewoo; Ji, Youngheum; Ju, Hyeonchang; Lee, Chang-Hun; Sung, Young Kwan; Kim, So Yeon; Moon, Cheil
Abstract: Introduction Hair loss (alopecia) is a multifactorial disorder that often causes distress. Approved therapies such as minoxidil and finasteride act indirectly and do not specifically target hair follicle (HF) cells. Erythropoietin (EPO), however, has been shown to activate dermal papilla (DP) cells via the erythropoietin receptor (EPOR), suggesting a potential role in hair follicle regeneration and hair growth. Objectives This study aimed to develop and validate Helix C-1–based EPO-derived peptides that activate DP cells and increase IGF-1 expression, while not inducing overt systemic erythropoietic effects (e.g., increases in red blood cell counts, reticulocytes, hemoglobin, or hematocrit) under the tested experimental conditions. Methods Peptides derived from the Helix C-1 region of EPO were synthesized and characterized by EPOR-binding affinity, CD spectroscopy, and ERK/AKT activation. In vitro, DP-cell metabolic activity, proliferation, and IGF-1 secretion were assessed. Ex vivo efficacy was evaluated by hair shaft elongation in hair follicle organ culture, and in vivo efficacy was tested in a murine depilation-induced anagen model with concurrent hematologic assessment to exclude erythropoiesis-related effects. Results The peptides increased DP-cell metabolic activity and proliferation, reduced oxidative stress, and enhanced IGF-1 production via EPOR-mediated ERK/AKT activation. They promoted hair shaft elongation ex vivo and promoted anagen entry in mice without significant changes in standard hematologic parameters under the tested dosing regimen. Conclusion These findings support the conclusion that MLPH promotes hair growth via an EPOR-linked, IGF-1–dependent mechanism in DP cells. Future pharmacokinetic and disease-model studies are warranted to evaluate its translational potential. © 2026 The Authors.</summary>
    <dc:date>2026-02-28T15:00:00Z</dc:date>
  </entry>
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