Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling

Okita, Tomonori; Kita, Satomi; Fukuda, Shiro; Fukuoka, Kazuya; Kawada-Horitani, Emi; Iioka, Masahito; Nakamura, Yuto; Fujishima, Yuya; Nishizawa, Hitoshi; Kawamori, Dan; Matsuoka, Taka‐aki; Maeda, Norikazu; Shimomura, Iichiro

doi:10.1016/j.isci.2022.105404

Cited by 7 publications

(9 citation statements)

References 43 publications

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“…T-cadherin is expressed at different levels in various cell types, including endothelial cells 18 . The UV-F2 cells that we used in this study expressed far fewer T-cadherin than intact endothelial cells in vivo 4 .…”

Section: Resultsmentioning

confidence: 99%

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Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin

Fujii,

Fujishima,

Kita

et al. 2024

Sci Rep

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Pharmacological activation of hypoxia-inducible factor 1 (HIF-1), a hypoxia-responsive transcription factor, has attracted increasing attention due to its efficacy not only in renal anemia but also in various disease models. Our study demonstrated that a HIF-1 activator enhanced extracellular vesicle (EV) production from cultured endothelial cells synergistically with adiponectin, an adipocyte-derived factor, through both transcriptional induction and posttranscriptional stabilization of an adiponectin binding partner, T-cadherin. Increased EV levels were observed in wild-type mice but not in T-cadherin null mice after consecutive administration of roxadustat. Adiponectin- and T-cadherin-dependent increased EV production may be involved in the pleiotropic effects of HIF-1 activators.

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Section: Resultsmentioning

confidence: 99%

“…Male C57BL/6J WT mice were purchased from CLEA Japan (Tokyo, Japan). T-cadherin KO mice were generated as previously described 18 and bred on a C57BL/6J background. Mice were housed in 22 ℃ at a 12-h light/12-h dark cycle (lights on from 8:00 A.M. to 8:00 P.M.).…”

Section: Methodsmentioning

confidence: 99%

Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin

Fujii,

Fujishima,

Kita

et al. 2024

Sci Rep

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“…In a previous study, we applied this system to increase circulating levels of C-type natriuretic peptide and verified the prolonged increase even at 4 weeks after transfection (25). Attempts to increase circulating protein levels with hydrodynamic gene delivery using pLIVE vectors were performed for fibroblast growth factor 21 (31, 32) and soluble T-cadherin (33). Kwon et al .…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Landscape of Hyperthyroidism in Mice Overexpressing Thyroid Stimulating Hormone

Yamauchi,

Sugawa,

Hakata

et al. 2023

Preprint

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Hyperthyroidism is a condition with excessive thyroid hormone secretion. Activation of thyroid stimulating hormone receptor (TSHR) fundamentally leads to hyperthyroidism. The details of TSHR signaling remain to be elucidated. We conducted transcriptome analyses for hyperthyroid mice that we generated by overexpressing TSH. TSH overexpression via hydrodynamic gene delivery with pLIVE-TSHBand pLIVE-CGAvectors consistently caused hyperthyroidism and goiters for at least 4 weeks in C57BL/6J mice. RNA sequencing analysis of their thyroid glands revealed that thiamazole slightly changed the thyroid transcriptome, which reinforces a conventional theory that thiamazole decreases thyroid hormone secretion via inhibition of thyroid peroxidase activity. Meanwhile, TSH overexpression drastically changed the thyroid transcriptome. In particular, enrichment analyses identified the cell cycle, phosphatidylinositol-3 kinase/Akt pathway, and Ras-related protein 1 pathway as possibly associated with goiter development. Regarding the role of TSHR signaling in hyperthyroidism, it is noteworthy thatSlc26a4was exclusively upregulated among genes crucial to thyroid hormone secretion at both 1 and 4 weeks after hydrodynamic gene delivery. To verify the relationship between this upregulation and hyperthyroidism, we overexpressed TSH inSlc26a4knockout mice. TSH overexpression caused hyperthyroidism inSlc26a4knockout mice, equivalent to that in control mice. To summarize, we analyzed hyperthyroid mice generated by TSH overexpression. We did not observe significant changes in known genes and pathways involved in thyroid hormone secretion. Thus, our datasets might include candidate genes that have not yet been identified as regulators of thyroid function. Our transcriptome datasets regarding hyperthyroidism can contribute to future research on TSHR signaling.

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“…T-cadherin is expressed at different levels in various cell types, including endothelial cells 15 . The UV-F2 cells that we used in this study expressed far fewer T-cadherin than intact endothelial cells in vivo 4 .…”

Section: Hif-1 Activation Stabilizes T-cadherin Protein In Cultured E...mentioning

confidence: 99%

“…Male C57BL/6J WT mice were purchased from CLEA Japan (Tokyo, Japan). T-cadherin KO mice were generated as previously described 15 and bred on a C57BL/6J background. Mice were housed in 22 ℃ at a 12-hour light/12-hour dark cycle (lights on from 8:00 AM to 8:00 PM).…”

Section: Animalsmentioning

confidence: 99%

Pharmacological HIF-1 activation upregulates exosome production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin

Fujii,

Fujishima,

Kita

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

Pharmacological activation of hypoxia-inducible factor 1alpha (HIF-1α), a hypoxia-responsive transcription factor, has attracted increasing attention due to its efficacy not only in renal anemia but also in various disease models. Our study demonstrated that a HIF-1 activator enhanced exosome production from cultured endothelial cells synergistically with adiponectin, an adipocyte-derived factor, through both transcriptional induction and posttranscriptional stabilization of an adiponectin binding partner, T-cadherin. Increased exosome levels were observed in wild-type mice but not in T-cadherin null mice after consecutive administration of roxadustat. Adiponectin- and T-cadherin-dependent increased exosome production may be involved in the pleiotropic effects of HIF-1 activators.

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Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling

Cited by 7 publications

References 43 publications

Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin

Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin

Transcriptomic Landscape of Hyperthyroidism in Mice Overexpressing Thyroid Stimulating Hormone

Pharmacological HIF-1 activation upregulates exosome production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin

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