Roles of Erythroid Differentiation Regulator 1 (Erdr1) on Inflammatory Skin Diseases

Houh, Youn Kyung; Kim, Kyung Eun; Park, Hyun Jeong; Cho, Daeho

doi:10.3390/ijms17122059

Cited by 18 publications

(19 citation statements)

References 67 publications

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“…In photodamaged skin, AKs, and cSCCs, evidence of the TP53 tumor suppressor protein was observed in keratinocytes and has been recorded in 69 to over 90% of invasive cSCC [20, 21]. Other implicated mutations in field cancerized islands include the oncogenes c-myc, Ras, H-ras, c-jun, WNT and KNSTRN and the tumor suppressors, p16INK4, NF-κB, Notch1, Notch2, Hes1 and Erdr1 [20, 16, 2, 22, 23]. Some studies have genotyped AKs and cSCC to identify potential key biomarkers which may be useful for diagnosis, prevention or treatment [24, 11, 25].…”

Section: Pathogenesismentioning

confidence: 99%

Updates on Treatment Approaches for Cutaneous Field Cancerization

et al. 2019

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Purpose of Review Field cancerization describes the phenomenon that multiple heterogenous mutations may arise in an area exposed to chronic carcinogenic stimuli. Advances in the understanding of cutaneous field cancerization have led to novel therapeutic approaches to the management of actinic keratoses (AKs). Herein, we review the literature on the pathophysiology and emerging research of field cancerization in dermatology. Recent Findings The classification systems for grading AK lesions are being refined with investigations focusing on their clinical utility. There is a growing shift towards field-directed treatment for AKs as the importance of field cancerization becomes clearer. Current field-directed therapies are being optimized and novel therapeutic modalities are being studied. Summary Field cancerization underlies the transformation of photodamaged skin into AKs and potentially cutaneous SCC (cSCC). Clinically meaningful classification systems for AKs are needed to better inform decisions regarding treatment. As we learn more about the role of field characterization in photodamage, AKs and cSCCs, therapeutic strategies are becoming more field-directed rather than lesion-directed.

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Section: Pathogenesismentioning

confidence: 99%

Updates on Treatment Approaches for Cutaneous Field Cancerization

et al. 2019

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“…Using this model, we focus on transcriptional changes in adult exGF mice that are irreversible by colonization with SPF microbiota. We identified one of the top-most differentially expressed genes between SPF and exGF mouse small intestine and colon to be erythroid differentiation regulator-1 (Erdr1), a soluble factor that regulates cellular survival, metastasis, and NK-mediated cytotoxicity 21,22 . Our findings show that Erdr1 is induced by microbiota in early life, localizes to Lgr5 + ISCs and TA cells and induces intestinal epithelial proliferation and regeneration in response to mucosal damage.…”

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confidence: 99%

Erythroid differentiation regulator-1 induced by microbiota in early life drives intestinal stem cell proliferation and regeneration

et al. 2020

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Gut microbiota and their metabolites are instrumental in regulating intestinal homeostasis. However, early-life microbiota associated influences on intestinal development remain incompletely understood. Here we demonstrate that co-housing of germ-free (GF) mice with specific-pathogen free (SPF) mice at weaning (exGF) results in altered intestinal gene expression. Our results reveal that one highly differentially expressed gene, erythroid differentiation regulator-1 (Erdr1), is induced during development in SPF but not GF or exGF mice and localizes to Lgr5 + stem cells and transit amplifying (TA) cells. Erdr1 functions to induce Wnt signaling in epithelial cells, increase Lgr5 + stem cell expansion, and promote intestinal organoid growth. Additionally, Erdr1 accelerates scratch-wound closure in vitro, increases Lgr5 + intestinal stem cell regeneration following radiation-induced injury in vivo, and enhances recovery from dextran sodium sulfate (DSS)-induced colonic damage. Collectively, our findings indicate that early-life microbiota controls Erdr1-mediated intestinal epithelial proliferation and regeneration in response to mucosal damage.

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“…Erythroid Differentiation Regulator 1 (Erdr1) is a cytokine which was initially known as a factor for hemoglobin synthesis in murine and human erythroleukemia cell lines [1]. This autocrine…”

Section: Erythroid Differentiation Regulatormentioning

confidence: 99%

Role of Erythroid Differentiation Regulator 1 (Erdr1) On Inflammatory Skin Disorders: A Review

AlSogair¹

2017

SM Dermatolog J

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A literature search was done on Pub med using the search terms "erythroid differentiation regulator 1" and "erdr1". The articles were later scanned for relevant data. The bibliographies of the articles were further examined for relevant references. All the evaluations were done by the author. Relevant data from twelve (12) articles were included in this review. Results Erythroid differentiation regulator 1Erythroid Differentiation Regulator 1 (Erdr1) is a cytokine which was initially known as a factor for hemoglobin synthesis in murine and human erythroleukemia cell lines [1]. This autocrine

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Roles of Erythroid Differentiation Regulator 1 (Erdr1) on Inflammatory Skin Diseases

Cited by 18 publications

References 67 publications

Updates on Treatment Approaches for Cutaneous Field Cancerization

Updates on Treatment Approaches for Cutaneous Field Cancerization

Erythroid differentiation regulator-1 induced by microbiota in early life drives intestinal stem cell proliferation and regeneration

Role of Erythroid Differentiation Regulator 1 (Erdr1) On Inflammatory Skin Disorders: A Review

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