Reichardt, Holger Michael

[["dc.bibliographiccitation.artnumber","1319"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Li, Xiao"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.date.accessioned","2019-07-09T11:44:30Z"],["dc.date.available","2019-07-09T11:44:30Z"],["dc.date.issued","2017"],["dc.description.abstract","Myeloid cells play an important role in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Monocytes, macrophages, and microglia can adopt two distinct phenotypes, with M1-polarized cells being more related to inflammation and autoimmunity while M2-polarized cells contribute to tissue repair and anti-inflammatory processes. Here, we show that deletion of the mineralocorticoid receptor (MR) in bone marrow-derived macrophages and peritoneal macrophages caused their polarization toward the M2 phenotype with its distinct gene expression, altered phagocytic and migratory properties, and dampened NO production. After induction of EAE, mice that are selectively devoid of the MR in their myeloid cells (MRlysM mice) showed diminished clinical symptoms and ameliorated histological hallmarks of neuroinflammation. T cells in peripheral lymphoid organs of these mice produced less pro-inflammatory cytokines while their proliferation and the abundance of regulatory T cells were unaltered. The numbers of inflammatory monocytes and reactive microglia in the central nervous system (CNS) in MRlysM mice were significantly lower and they adopted an M2-polarized phenotype based on their gene expression profile, presumably explaining the ameliorated neuroinflammation. Our results indicate that the MR in myeloid cells plays a critical role for CNS autoimmunity, providing a rational to interfere with diseases such as MS by pharmacologically targeting this receptor."],["dc.identifier.doi","10.3389/fimmu.2017.01319"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14800"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59025"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Deletion of the Mineralocorticoid Receptor in Myeloid Cells Attenuates Central Nervous System Autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15437"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","15450"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Baake, Tina"],["dc.contributor.author","Jörß, Katharina"],["dc.contributor.author","Suennemann, Jennifer"],["dc.contributor.author","Roßmann, Laura"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:14Z"],["dc.date.available","2019-07-09T11:45:14Z"],["dc.date.issued","2018"],["dc.description.abstract","Graft-versus-host disease (GvHD) is a life-threatening complication of hematopoietic stem cell transplantation (HSCT), which is caused by allogeneic T cells recognizing molecules of the recipient as foreign. Endogenous glucocorticoids (GC) released from the adrenal gland are crucial in regulating such inflammatory diseases. Here we demonstrate that genetically engineered mice, that are largely unresponsive to GC, suffer from aggravated clinical symptoms and increased mortality after HSCT, effects that could be tempered by neutralization of IL-6. Interestingly, selective ablation of the GC receptor (GR) in recipient myeloid cells resulted in fulminant disease as well. While histopathological analysis of the jejunum failed to reveal any differences between sick mice of both genotypes, systemic IL-6 and TNFα secretion was strongly increased in transplanted mice lacking the GR in myeloid cells briefly before the majority of them succumbed to the disease. Collectively, our findings reveal an important role of the GR in recipient cells in limiting the cytokine storm caused by GvHD induction."],["dc.identifier.doi","10.18632/oncotarget.24602"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15071"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59189"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","The glucocorticoid receptor in recipient cells keeps cytokine secretion in acute graft-versus-host disease at bay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","14"],["dc.contributor.author","Hoepner, Robert"],["dc.contributor.author","Bagnoud, Maud"],["dc.contributor.author","Pistor, Maximilian"],["dc.contributor.author","Salmen, Anke"],["dc.contributor.author","Briner, Myriam"],["dc.contributor.author","Synn, Helen"],["dc.contributor.author","Schrewe, Lisa"],["dc.contributor.author","Guse, Kirsten"],["dc.contributor.author","Ahmadi, Farhad"],["dc.contributor.author","Demir, Seray"],["dc.contributor.author","Laverick, Louis"],["dc.contributor.author","Gresle, Melissa"],["dc.contributor.author","Worley, Paul"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Butzkueven, Helmut"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2019-07-09T11:51:33Z"],["dc.date.available","2019-07-09T11:51:33Z"],["dc.date.issued","2019"],["dc.description.abstract","The limited efficacy of glucocorticoids (GCs) during therapy of acute relapses in multiple sclerosis (MS) leads to long-term disability. We investigated the potential of vitamin D (VD) to enhance GC efficacy and the mechanisms underlying this VD/GC interaction. In vitro, GC receptor (GR) expression levels were quantified by ELISA and induction of T cell apoptosis served as a functional readout to assess synergistic 1,25(OH)2D3 (1,25D)/GC effects. Experimental autoimmune encephalomyelitis (MOG35-55 EAE) was induced in mice with T cell-specific GR or mTORc1 deficiency. 25(OH)D (25D) levels were determined in two independent cohorts of MS patients with stable disease or relapses either responsive or resistant to GC treatment (initial cohort: n = 110; validation cohort: n = 85). Gene expression of human CD8+ T cells was analyzed by microarray (n = 112) and correlated with 25D serum levels. In vitro, 1,25D upregulated GR protein levels, leading to increased GC-induced T cell apoptosis. 1,25D/GC combination therapy ameliorated clinical EAE course more efficiently than respective monotherapies, which was dependent on GR expression in T cells. In MS patients from two independent cohorts, 25D deficiency was associated with GC-resistant relapses. Mechanistic studies revealed that synergistic 1,25D/GC effects on apoptosis induction were mediated by the mTOR but not JNK pathway. In line, 1,25D inhibited mTORc1 activity in murine T cells, and low 25D levels in humans were associated with a reduced expression of mTORc1 inhibiting tuberous sclerosis complex 1 in CD8+ T cells. GR upregulation by 1,25D and 1,25D/GC synergism in vitro and therapeutic efficacy in vivo were abolished in animals with a T cell-specific mTORc1 deficiency. Specific inhibition of mTORc1 by everolimus increased the efficacy of GC in EAE. 1,25D augments GC-mediated effects in vitro and in vivo in a T cell-specific, GR-dependent manner via mTORc1 inhibition. These data may have implications for improvement of anti-inflammatory GC therapy."],["dc.identifier.doi","10.1007/s00401-019-02018-8"],["dc.identifier.pmid","31030237"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16149"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59968"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1432-0533"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Vitamin D increases glucocorticoid efficacy via inhibition of mTORC1 in experimental models of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","International journal of molecular sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Lühder, Fred; \t\t \r\n\t\t Institute of Neuroimmunology and Institute for Multiple Sclerosis Research, University Medical Centre Goettingen, 37075 Göttingen, Germany, fred.luehder@med.uni-goettingen.de"],["dc.contributor.affiliation","Reichardt, Holger; \t\t \r\n\t\t Institute for Cellular and Molecular Immunology, University Medical Center Goettingen, 37073 Göttingen, Germany, hreichardt@med.uni-goettingen.de"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2019-07-09T11:43:39Z"],["dc.date.available","2019-07-09T11:43:39Z"],["dc.date.issued","2017-08-24"],["dc.date.updated","2022-09-06T05:11:07Z"],["dc.description.abstract","Glucocorticoids (GC) are one of the most popular and versatile classes of drugs available to treat chronic inflammation and cancer, but side effects and resistance constrain their use. To overcome these hurdles, which are often related to the uniform tissue distribution of free GC and their short half-life in biological fluids, new delivery vehicles have been developed including PEGylated liposomes, polymeric micelles, polymer-drug conjugates, inorganic scaffolds, and hybrid nanoparticles. While each of these nanoformulations has individual drawbacks, they are often superior to free GC in many aspects including therapeutic efficacy when tested in cell culture or animal models. Successful application of nanomedicines has been demonstrated in various models of neuroinflammatory diseases, cancer, rheumatoid arthritis, and several other disorders. Moreover, investigations using human cells and first clinical trials raise the hope that the new delivery vehicles may have the potential to make GC therapies more tolerable, specific and efficient in the future."],["dc.identifier.doi","10.3390/ijms18091836"],["dc.identifier.pmid","28837059"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14615"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58940"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Novel Drug Delivery Systems Tailored for Improved Administration of Glucocorticoids."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0190846"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Meers, Garrit K."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:08Z"],["dc.date.available","2019-07-09T11:45:08Z"],["dc.date.issued","2018"],["dc.description.abstract","Inflammatory bowel disease (IBD) is a highly prevalent intestinal disorder for which no cure exists. Currently, the standard first-line treatment of IBD consists of systemic glucocorticoid (GC) application, even though therapy can be complicated by unresponsiveness or adverse effects. In view of the importance of macrophages and neutrophils for the pathogenesis of IBD we set out to define the relevance of these cell types as targets of GC using the mouse model of DSS-induced colitis. We found that the disease did not resolve in GRlysM mice lacking the GC receptor (GR) in myeloid cells after removal of the chemical insult. While clinical symptoms and tissue damage in the colon ameliorated again in GRflox mice, the disease further aggravated in GRlysM littermates. The observed difference coincided with an increased abundance of macrophages in inflammatory infiltrates in the colon of mutant mice whereas neutrophil and T cell numbers were similar. Concomitantly, systemic IL-6 secretion and mRNA levels of pro-inflammatory cytokines in the colon were elevated in GRlysM mice and gene expression of scavenger receptors and IL-10 was diminished. Taken together, our results reveal an important role of myeloid cells as targets of GC in DSS-induced colitis and probably in IBD in humans as well."],["dc.identifier.doi","10.1371/journal.pone.0190846"],["dc.identifier.pmid","29324769"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59164"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Colitis"],["dc.subject.mesh","Colon"],["dc.subject.mesh","Dextran Sulfate"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Interleukin-10"],["dc.subject.mesh","Interleukin-6"],["dc.subject.mesh","Intestinal Mucosa"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Myeloid Cells"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Receptors, Glucocorticoid"],["dc.title","Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8434"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of immunology (Baltimore, Md. : 1950)"],["dc.bibliographiccitation.lastpage","8443"],["dc.bibliographiccitation.volume","180"],["dc.contributor.author","Wüst, Simone"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Kleiman, Anna"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2019-07-10T08:13:33Z"],["dc.date.available","2019-07-10T08:13:33Z"],["dc.date.issued","2008"],["dc.description.abstract","High-dose glucocorticoid (GC) therapy is widely used to treat multiple sclerosis (MS), but the underlying mechanisms remain debatable. In this study, we investigated the impact of GC administration on experimental autoimmune encephalomyelitis using different GC receptor (GR)-deficient mutants. Heterozygous GR knockout mice were less sensitive to dexamethasone therapy, indicating that the expression level of the receptor determines therapeutic efficacy. Mice reconstituted with homozygous GR knockout fetal liver cells showed an earlier onset of the disease and were largely refractory to GC treatment, indicating that the GR in hematopoietic cells is essential for the beneficial effects of endogenous GCs and dexamethasone. Using cell-type specific GR-deficient mice, we could demonstrate that GCs mainly act on T cells, while modulation of macrophage function was largely dispensable in this context. The therapeutic effects were achieved through induction of apoptosis and down-regulation of cell adhesion molecules in peripheral T(H)17 and bystander T cells, while similar effects were not observed within the spinal cord. In addition, dexamethasone inhibited T cell migration into the CNS, confirming that peripheral but not CNS-residing T lymphocytes are the essential targets of GCs. Collectively, our findings reveal a highly selective mechanism of GC action in experimental autoimmune encephalomyelitis and presumably multiple sclerosis."],["dc.identifier.pmid","18523311"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61275"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","0022-1767"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Blood-Brain Barrier"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Dexamethasone"],["dc.subject.mesh","Down-Regulation"],["dc.subject.mesh","Drug Delivery Systems"],["dc.subject.mesh","Encephalomyelitis, Autoimmune, Experimental"],["dc.subject.mesh","Female"],["dc.subject.mesh","Glycoproteins"],["dc.subject.mesh","Intercellular Signaling Peptides and Proteins"],["dc.subject.mesh","Leukocytes"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Knockout"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Peptide Fragments"],["dc.subject.mesh","Receptors, Glucocorticoid"],["dc.subject.mesh","T-Lymphocyte Subsets"],["dc.subject.mesh","T-Lymphocytes, Regulatory"],["dc.title","Peripheral T cells are the therapeutic targets of glucocorticoids in experimental autoimmune encephalomyelitis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1200"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Finck, Tobias L. K."],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.date.accessioned","2019-07-09T11:51:45Z"],["dc.date.available","2019-07-09T11:51:45Z"],["dc.date.issued","2019"],["dc.description.abstract","Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS), characterized by the infiltration of mononuclear cells into the CNS and a subsequent inflammation of the brain.Monocytes are implicated in disease pathogenesis not only in their function as potential antigen-presenting cells involved in the local reactivation of encephalitogenic T cells but also by independent effector functions contributing to structural damage and disease progression. However, monocytes also have beneficial effects as they can exert anti-inflammatory activity and promote tissue repair. Glucocorticoids (GCs) are widely used to treat acute relapses in MS patients. They act on a variety of cell types but their exact mechanisms of action including their modulation of monocyte function are not fully understood. Here we investigated effects of the therapeutically relevant GC methylprednisolone (MP) on monocytes from healthy individuals and MS patients in vitro and in vivo. The monocyte composition in the blood was different in MS patients compared to healthy individuals, but it was only marginally affected byMP treatment. In contrast, application ofMP caused amarked shift toward an anti-inflammatory monocyte phenotype in vitro and in vivo as revealed by an altered gene expression profile. Chemotaxis of monocytes toward CCL2, CCL5, and CX3CL1 was increased in MS patients compared to healthy individuals and further enhanced by MP pulse therapy. Both of these migration-promoting effects were more pronounced in MS patients with an acute relapse than in those with a progressive disease. Interestingly, the pro-migratory GC effect was independent of chemokine receptor levels as exemplified by results obtained for CCR2. Collectively, our findings suggest that GCs polarizemonocytes toward an anti-inflammatory phenotype and enhance their migration into the inflamed CNS, endowing them with the capacity to suppress the pathogenic immune response."],["dc.identifier.doi","10.3389/fimmu.2019.01200"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60002"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Glucocorticoid Therapy of Multiple Sclerosis Patients Induces Anti-inflammatory Polarization and Increased Chemotaxis of Monocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","731"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","FASEB BioAdvances"],["dc.bibliographiccitation.lastpage","746"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Markov, Alex"],["dc.contributor.author","Kraemer, Lena K."],["dc.contributor.author","Christalla, Peter"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2020-01-21T09:29:21Z"],["dc.date.accessioned","2021-10-27T13:22:07Z"],["dc.date.available","2020-01-21T09:29:21Z"],["dc.date.available","2021-10-27T13:22:07Z"],["dc.date.issued","2019"],["dc.description.abstract","Satellite cells reside in defined niches and are activated upon skeletal muscle injury to facilitate regeneration. Mechanistic studies of skeletal muscle regeneration are hampered by the inability to faithfully simulate satellite cell biology in vitro. We sought to overcome this limitation by developing tissue engineered skeletal muscle (ESM) with (1) satellite cell niches and (2) the capacity to regenerate after injury. ESMs contained quiescent Pax7‐positive satellite cells in morphologically defined niches. Satellite cells could be activated to repair (i) cardiotoxin and (ii) mechanical crush injuries. Activation of the Wnt‐pathway was essential for muscle regeneration. Finally, muscle progenitors from the engineered niche developed de novo ESM in vitro and regenerated skeletal muscle after cardiotoxin‐induced injury in vivo. We conclude that ESM with functional progenitor niches reminiscent of the in vivo satellite cell niches can be engineered in vitro. ESM may ultimately be exploited in disease modeling, drug screening, or muscle regeneration."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2019"],["dc.identifier.doi","10.1096/fba.2019-00013"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17135"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92070"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2573-9832"],["dc.relation.issn","2573-9832"],["dc.relation.issn","2573-9832"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Regeneration competent satellite cell niches in rat engineered skeletal muscle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]