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We are analyzing https://link.springer.com/article/10.1007/s00018-021-04031-1.

Title:
Development of a novel and synthetic HematoMiR technology that broadly modulates quiescence of stem cells and enhances HSC expansion | Cellular and Molecular Life Sciences
Description:
Hematopoietic stem cell (HSCs) transplantation is the primary therapeutic modality used to treat hematopoietic disorders. It centers on the capability of a small quantity of HSCs to repopulate whole blood lineages. Along with limited availability of suitable donors, the need for sufficient number of donor HSCs is still challenging in clinical relevance. This has been addressed by ex vivo HSC expansion albeit with partial success, and thus development of an alternative strategy that could improve HSC expansion is required. To that end, we aimed to build HematoMiR, an oligo-based technology that broadly targets HSC quiescence factors. Here, we show that HematoMiRs and their combinations targeting over 50 factors involved in HSC quiescence could induce robust ex vivo murine and human HSC expansion. In particular, HematoMiR-5 treatment enhanced cell cycle through down-regulation of negative cell cycle regulators in HSCs. HematoMiR-5 treated HSPCs had reduced DNA damage during the course of ex vivo expansion. Moreover, HematoMiR-5 treatment led to sustained HSC self-renewal ability and a low apoptosis rate. In addition, HematoMiR-5 expanded HSCs demonstrated successful engraftment and repopulation capacity in the recipient animals. Furthermore, combinatorial treatments of HematoMiR-2 and 5 allowed vigorous ex vivo HSC expansion. These findings demonstrate that novel and synthetic HematoMiR technology is feasible for HSC ex vivo expansion through the sequence-dependent modulation of numerous HSC quiescence modulators. Graphical abstract
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

pubmed, article, google, scholar, cas, stem, cell, cells, central, hematopoietic, expansion, hsc, vivo, mol, blood, expression, quiescence, biol, nature, hematomir, transplantation, sci, microrna, human, med, httpsdoiorgs, regulation, data, kocabaş, cycle, engraftment, nucleic, acids, uslu, dna, gene, httpsdoiorgjstem, res, privacy, cookies, content, analysis, information, development, hscs, factors, selfrenewal, access, haematopoietic, kocabas,

Topics {✒️}

mir-466f-3p sustains epithelial month download article/chapter vivo haematopoietic-stem-cell expansion dna double-strand breaks vegfa-nrp2 signaling pathway haematopoietic stem cells transcription factors foxo rna-binding protein hur human haematopoietic stem satb2-induced osteogenic differentiation transplant dose-regulated expansion hematopoietic stem cells regulating il-10/il-12 levels stress-induced terminal differentiation article uslu stem cell quiescence purified stem cells broadly modulates quiescence full article pdf immune regulatory cells microrna–target interactions limited availability mesenchymal transition cell cycle quiescence human hematopoietic stem cell cycle regulated deconstructing stem cell dose-response surface analysis early hematopoietic recovery cytokine signals modulated sequence-dependent modulation fatih kocabaş checkpoint activation privacy choices/manage cookies article number 68 long-term engraftment potential cell-cycle regulation progenitor cells revealed microrna binding sites acute liver failure leukaemia-initiating cells enhances hsc expansion mir-125a-5p microrna expression signature microrna expression correlates hematopoietic cell transplantation stem cells stem cells 1185 treat hematopoietic disorders hematomir-5 treatment led

Schema {🗺️}

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         description:Hematopoietic stem cell (HSCs) transplantation is the primary therapeutic modality used to treat hematopoietic disorders. It centers on the capability of a small quantity of HSCs to repopulate whole blood lineages. Along with limited availability of suitable donors, the need for sufficient number of donor HSCs is still challenging in clinical relevance. This has been addressed by ex vivo HSC expansion albeit with partial success, and thus development of an alternative strategy that could improve HSC expansion is required. To that end, we aimed to build HematoMiR, an oligo-based technology that broadly targets HSC quiescence factors. Here, we show that HematoMiRs and their combinations targeting over 50 factors involved in HSC quiescence could induce robust ex vivo murine and human HSC expansion. In particular, HematoMiR-5 treatment enhanced cell cycle through down-regulation of negative cell cycle regulators in HSCs. HematoMiR-5 treated HSPCs had reduced DNA damage during the course of ex vivo expansion. Moreover, HematoMiR-5 treatment led to sustained HSC self-renewal ability and a low apoptosis rate. In addition, HematoMiR-5 expanded HSCs demonstrated successful engraftment and repopulation capacity in the recipient animals. Furthermore, combinatorial treatments of HematoMiR-2 and 5 allowed vigorous ex vivo HSC expansion. These findings demonstrate that novel and synthetic HematoMiR technology is feasible for HSC ex vivo expansion through the sequence-dependent modulation of numerous HSC quiescence modulators.
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External Links {🔗}(372)

Analytics and Tracking {📊}

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Libraries {📚}

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CDN Services {📦}

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