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Book: microRNAs in endocrine cancers and metabolism

Krützfeldt, Jan

(Best practice & research. Clinical endocrinology & metabolism ; volume 30, issue 5 (October 2016))

2016

Author's details	Jan Krützfeldt, guest editor
Series title	Best practice & research. Clinical endocrinology & metabolism ; volume 30, issue 5 (October 2016) Best practice & research
Collection	Best practice & research
Language	English
Size	Seiten 549-676, Illustrationen
Publisher	Elsevier
Publishing place	Amsterdam
Publishing country	Netherlands
Document type	Book
HBZ-ID	HT019209560
Database	Catalogue ZB MED Medicine, Health

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Article: Hormonelle Ursachen des vermehrten Schwitzens.

Krützfeldt, Jan

Praxis

2023 Volume 112, Issue 7-8, Page(s) 398–402

Abstract: Hormonal Causes for Excessive ... ...

Title translation	Hormonal Causes for Excessive Sweating.
Abstract	Hormonal Causes for Excessive Sweating
MeSH term(s)	Female ; Humans ; Male ; Sweating ; Menopause ; Aging
Language	German
Publishing date	2023-06-07
Publishing country	Switzerland
Document type	English Abstract ; Journal Article
ZDB-ID	209026-0
ISSN	1661-8165 ; 1661-8157 ; 0369-8394
ISSN (online)	1661-8165
ISSN	1661-8157 ; 0369-8394
DOI	10.1024/1661-8157/a004025
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Article ; Online: microRNA-501 controls myogenin

Fahrner, Alexandra / Luca, Edlira / Krützfeldt, Jan

Molecular metabolism

2023 Volume 71, Page(s) 101704

Abstract: Objective: Skeletal muscle regeneration is markedly impaired during aging. How adult muscle stem cells contribute to this decrease in regenerative capacity is incompletely understood. We investigated mechanisms of age-related changes in myogenic ... ...

Abstract	Objective: Skeletal muscle regeneration is markedly impaired during aging. How adult muscle stem cells contribute to this decrease in regenerative capacity is incompletely understood. We investigated mechanisms of age-related changes in myogenic progenitor cells using the tissue-specific microRNA 501. Methods: Young and old C57Bl/6 mice were used (3 months or 24 months of age, respectively) with or without global or tissue-specific genetic deletion of miR-501. Muscle regeneration was induced using intramuscular cardiotoxin injection or treadmill exercise and analysed using single cell and bulk RNA sequencing, qRT-PCR and immunofluorescence. Muscle fiber damage was assessed with Evan`s blue dye (EBD). In vitro analysis was performed in primary muscle cells obtained from mice and humans. Results: Single cell sequencing revealed myogenic progenitor cells in miR-501 knockout mice at day 6 after muscle injury that are characterized by high levels of myogenin and CD74. In control mice these cells were less in number and already downregulated after day 3 of muscle injury. Muscle from knockout mice had reduced myofiber size and reduced myofiber resilience to injury and exercise. miR-501 elicits this effect by regulating sarcomeric gene expression through its target gene estrogen-related receptor gamma (Esrrg). Importantly, in aged skeletal muscle where miR-501 was significantly downregulated and its target Esrrg significantly upregulated, the number of myog Conclusions: miR-501 and Esrrg are regulated in muscle with decreased regenerative capacity and loss of miR-501 is permissive to the appearance of CD74
MeSH term(s)	Adult ; Aged ; Animals ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Skeletal/metabolism ; Myogenin/genetics ; Myogenin/metabolism ; Myogenin/pharmacology ; Regeneration/genetics ; Stem Cells/metabolism
Chemical Substances	MicroRNAs ; MIRN501 microRNA, human ; Myogenin ; MIRN501 microRNA, mouse
Language	English
Publishing date	2023-03-11
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2023.101704
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Article ; Online: Preface - microRNAs in endocrine cancers and metabolism.

Krützfeldt, Jan

Best practice & research. Clinical endocrinology & metabolism

2016 Volume 30, Issue 5, Page(s) 549

Language	English
Publishing date	2016-10
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2016.11.011
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Article ; Online: Strategies to use microRNAs as therapeutic targets.

Krützfeldt, Jan

Best practice & research. Clinical endocrinology & metabolism

2016 Volume 30, Issue 5, Page(s) 551–561

Abstract: MicroRNAs (miRNAs) provide a unique mechanism of gene regulation and play a key role in different pathologies ranging from metabolic diseases to cancer. miRNAs can impact biological function as either suppressors of gene expression when their expression ... ...

Abstract	MicroRNAs (miRNAs) provide a unique mechanism of gene regulation and play a key role in different pathologies ranging from metabolic diseases to cancer. miRNAs can impact biological function as either suppressors of gene expression when their expression levels are enhanced in a disease state or they can cause upregulation of gene expression when their expression levels are reduced. Therefore both gain- and loss-of- function strategies are needed to fully exploit their therapeutic potential. miRNA research first focused on inhibition of single miRNAs using oligonucleotide inhibitors. However, more recent approaches explore the potential to deliver oligonucleotides to mimic miRNA expression or to employ small molecules to increase or inhibit miRNA function. Although we need to know more about the potential side effects and tissue specific delivery systems, these studies provide grounds to further exploit miRNAs as novel therapeutic targets in the clinic.
MeSH term(s)	Animals ; Gene Silencing ; Genetic Therapy/methods ; Humans ; Metabolic Diseases/genetics ; Metabolic Diseases/therapy ; MicroRNAs/drug effects ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasms/genetics ; Neoplasms/therapy ; Oligonucleotides/pharmacology ; Oligonucleotides/therapeutic use
Chemical Substances	MicroRNAs ; Oligonucleotides
Language	English
Publishing date	2016-10
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2016.07.004
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Article ; Online: Growth hormone/IGF-I-dependent signaling restores decreased expression of the myokine SPARC in aged skeletal muscle.

Mathes, Sebastian / Fahrner, Alexandra / Luca, Edlira / Krützfeldt, Jan

Journal of molecular medicine (Berlin, Germany)

2022 Volume 100, Issue 11, Page(s) 1647–1658

Abstract: Skeletal muscle exerts many beneficial effects on the human body including the contraction-dependent secretion of peptides termed myokines. We have recently connected the myokine secreted protein acidic and rich in cysteine (SPARC) to the formation of ... ...

Abstract	Skeletal muscle exerts many beneficial effects on the human body including the contraction-dependent secretion of peptides termed myokines. We have recently connected the myokine secreted protein acidic and rich in cysteine (SPARC) to the formation of intramuscular adipose tissue (IMAT) in skeletal muscle from aged mice and humans. Here, we searched for inducers of SPARC in order to uncover novel treatment approaches for IMAT. Endurance exercise in mice as well as forskolin treatment in vitro only modestly activated SPARC levels. However, through pharmacological treatments in vitro, we identified IGF-I as a potent inducer of SPARC expression in muscle cells, likely through a direct activation of its promoter via phosphatidylinositol 4,5-bisphospate 3-kinase (PI3K)-dependent signaling. We employed two different mouse models of growth hormone (GH)/IGF-I deficiency to solidify our understanding of the relationship between IGF-I and SPARC in vivo. GH administration robustly increased intramuscular SPARC levels (3.5-fold) in GH releasing hormone receptor-deficient mice and restored low intramuscular SPARC expression in skeletal muscle from aged mice. Intramuscular glycerol injections induced higher levels of adipocyte markers (adiponectin, perilipin) in aged compared to young mice, which was not prevented by GH treatment. Our study provides a roadmap for the study of myokine regulation during aging and demonstrates that the GH/IGF-I axis is critical for SPARC expression in skeletal muscle. Although GH treatment did not prevent IMAT formation in the glycerol model, targeting SPARC by exercise or by activation of IGF-I signaling might offer a novel therapeutic strategy against IMAT formation during aging. KEY MESSAGES : IGF-I regulates the myokine SPARC in muscle cells directly at the promoter level. GH/IGF-I is able to restore the decreased SPARC levels in aged skeletal muscle. The glycerol model induces higher adipocyte markers in aged compared to young muscle. GH treatment does not prevent IMAT formation in the glycerol model.
MeSH term(s)	Animals ; Mice ; Adiponectin/metabolism ; Colforsin/metabolism ; Cysteine ; Glycerol/metabolism ; Growth Hormone/metabolism ; Insulin-Like Growth Factor I ; Muscle, Skeletal/metabolism ; Osteonectin/genetics ; Osteonectin/metabolism ; Perilipins/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Physical Conditioning, Animal
Chemical Substances	Adiponectin ; Colforsin (1F7A44V6OU) ; Cysteine (K848JZ4886) ; Glycerol (PDC6A3C0OX) ; Growth Hormone (9002-72-6) ; Insulin-Like Growth Factor I (67763-96-6) ; Osteonectin ; Perilipins ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; SPARC protein, mouse
Language	English
Publishing date	2022-09-30
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-022-02260-w
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Article ; Online: microRNA-501 controls myogenin+/CD74+ myogenic progenitor cells during muscle regeneration

Alexandra Fahrner / Edlira Luca / Jan Krützfeldt

Molecular Metabolism, Vol 71, Iss , Pp 101704- (2023)

2023

Abstract	Objective: Skeletal muscle regeneration is markedly impaired during aging. How adult muscle stem cells contribute to this decrease in regenerative capacity is incompletely understood. We investigated mechanisms of age-related changes in myogenic progenitor cells using the tissue-specific microRNA 501. Methods: Young and old C57Bl/6 mice were used (3 months or 24 months of age, respectively) with or without global or tissue-specific genetic deletion of miR-501. Muscle regeneration was induced using intramuscular cardiotoxin injection or treadmill exercise and analysed using single cell and bulk RNA sequencing, qRT-PCR and immunofluorescence. Muscle fiber damage was assessed with Evan`s blue dye (EBD). In vitro analysis was performed in primary muscle cells obtained from mice and humans. Results: Single cell sequencing revealed myogenic progenitor cells in miR-501 knockout mice at day 6 after muscle injury that are characterized by high levels of myogenin and CD74. In control mice these cells were less in number and already downregulated after day 3 of muscle injury. Muscle from knockout mice had reduced myofiber size and reduced myofiber resilience to injury and exercise. miR-501 elicits this effect by regulating sarcomeric gene expression through its target gene estrogen-related receptor gamma (Esrrg). Importantly, in aged skeletal muscle where miR-501 was significantly downregulated and its target Esrrg significantly upregulated, the number of myog+/CD74+ cells during regeneration was upregulated to similar levels as observed in 501 knockout mice. Moreover, myog+/CD74+-aged skeletal muscle exhibited a similar decrease in the size of newly formed myofibers and increased number of necrotic myofibers after injury as observed in mice lacking miR-501. Conclusions: miR-501 and Esrrg are regulated in muscle with decreased regenerative capacity and loss of miR-501 is permissive to the appearance of CD74+ myogenic progenitors. Our data uncover a novel link between the metabolic transcription factor Esrrg and sarcomere ...
Keywords	microRNA ; aging ; Esrrg ; CD74 ; skeletal muscle ; regeneration ; Internal medicine ; RC31-1245
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Altered Distribution of Unesterified Cholesterol among Lipoprotein Subfractions of Patients with Diabetes Mellitus Type 2.

Kolb, Livia Noemi / Othman, Alaa / Rohrer, Lucia / Krützfeldt, Jan / von Eckardstein, Arnold

Biomolecules

2023 Volume 13, Issue 3

Abstract: Biomarkers are important tools to improve the early detection of patients at high risk for developing diabetes as well as the stratification of diabetic patients towards risks of complications. In addition to clinical variables, we analyzed 155 metabolic ...

Abstract	Biomarkers are important tools to improve the early detection of patients at high risk for developing diabetes as well as the stratification of diabetic patients towards risks of complications. In addition to clinical variables, we analyzed 155 metabolic parameters in plasma samples of 51 healthy volunteers and 66 patients with diabetes using nuclear magnetic resonance (NMR) spectrometry. Upon elastic net analysis with lasso regression, we confirmed the independent associations of diabetes with branched-chain amino acids and lactate (both positive) as well as linoleic acid in plasma and HDL diameter (both inverse). In addition, we found the presence of diabetes independently associated with lower concentrations of free cholesterol in plasma but higher concentrations of free cholesterol in small HDL. Compared to plasmas of non-diabetic controls, plasmas of diabetic subjects contained lower absolute and relative concentrations of free cholesterol in all LDL and HDL subclasses except small HDL but higher absolute and relative concentrations of free cholesterol in all VLDL subclasses (except very small VLDL). These disbalances may reflect disturbances in the transfer of free cholesterol from VLDL to HDL during lipolysis and in the transfer of cell-derived cholesterol from small HDL via larger HDL to LDL.
MeSH term(s)	Humans ; Lipoproteins ; Cholesterol ; Diabetes Mellitus, Type 2 ; Triglycerides ; Lipoproteins, LDL
Chemical Substances	Lipoproteins ; Cholesterol (97C5T2UQ7J) ; Triglycerides ; Lipoproteins, LDL
Language	English
Publishing date	2023-03-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13030497
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Article ; Online: Activation of PDGF Signaling in the Adult Muscle Stem Cell Niche in Patients With Type 2 Diabetes Mellitus.

Fahrner, Alexandra / Alchus Laiferová, Nikoleta / Ukropcová, Barbara / Ukropec, Jozef / Krützfeldt, Jan

The Journal of clinical endocrinology and metabolism

2023 Volume 108, Issue 8, Page(s) 2052–2064

Abstract: Context: Type 2 diabetes mellitus (T2D) negatively affects muscle mass and function throughout life. Whether adult muscle stem cells contribute to the decrease in muscle health is not clear and insights into the stem cell niche are difficult to obtain.!# ...

Abstract	Context: Type 2 diabetes mellitus (T2D) negatively affects muscle mass and function throughout life. Whether adult muscle stem cells contribute to the decrease in muscle health is not clear and insights into the stem cell niche are difficult to obtain. Objective: To establish the upstream signaling pathway of microRNA (miR)-501, a marker of activated myogenic progenitor cells, and interrogate this pathway in muscle biopsies from patients with T2D. Methods: Analysis of primary muscle cell cultures from mice and 4 normoglycemic humans and muscle biopsies from 7 patients with T2D and 7 normoglycemic controls using gene expression, information on histone methylation, peptide screening, and promoter assays. Results: miR-501 shares the promoter of its host gene, isoform 2 of chloride voltage-gated channel 5 (CLCN5-2), and miR-501 expression increases during muscle cell differentiation. We identify platelet-derived growth factor (PDGF) as an upstream regulator of CLCN5-2 and miR-501 via Janus kinase/signal transducer and activator of transcription. Skeletal muscle biopsies from patients with T2D revealed upregulation of PDGF (1.62-fold, P = .002), CLCN5-2 (2.85-fold, P = .03), and miR-501 (1.73-fold, P = .02) compared with normoglycemic controls. In addition, we observed a positive correlation of PDGF and miR-501 in human skeletal muscle (r = 0.542, P = .045, n = 14). Conclusions: We conclude that paracrine signaling in the adult muscle stem cells niche is activated in T2D. Expression analysis of the PDGF-miR-501 signaling pathway could represent a powerful tool to classify patients in clinical trials that aim to improve muscle health and glucose homeostasis in patients with diabetes.
MeSH term(s)	Adult ; Animals ; Humans ; Mice ; Diabetes Mellitus, Type 2 ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Skeletal/metabolism ; Platelet-Derived Growth Factor/metabolism ; Signal Transduction ; Stem Cell Niche
Chemical Substances	MicroRNAs ; Platelet-Derived Growth Factor
Language	English
Publishing date	2023-01-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad041
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Article ; Online: Uncoupling protein 1 expression in adipocytes derived from skeletal muscle fibro/adipogenic progenitors is under genetic and hormonal control.

Gorski, Tatiane / Mathes, Sebastian / Krützfeldt, Jan

Journal of cachexia, sarcopenia and muscle

2018 Volume 9, Issue 2, Page(s) 384–399

Abstract: Background: Intramuscular fatty infiltration is generally associated with the accumulation of white adipocytes in skeletal muscle and unfavourable metabolic outcomes. It is, however, still unclear whether intramuscular adipocytes could also acquire a ... ...

Abstract	Background: Intramuscular fatty infiltration is generally associated with the accumulation of white adipocytes in skeletal muscle and unfavourable metabolic outcomes. It is, however, still unclear whether intramuscular adipocytes could also acquire a brown-like phenotype. Here, we detected intramuscular expression of brown adipocyte markers during fatty infiltration in an obesity-resistant mouse strain and extensively compared the potential of two different stem cell populations residing in skeletal muscle to differentiate into brown-like adipocytes. Methods: Fatty infiltration was induced using intramuscular glycerol or cardiotoxin injection in the tibialis anterior muscles of young or aged 129S6/SvEvTac (Sv/129) mice or interleukin-6 (IL-6) knockout mice, and the expression of general and brown adipocyte markers was assessed after 4 weeks. Fibro/adipogenic progenitors (FAPs) and myogenic progenitors were prospectively isolated using fluorescence-activated cell sorting from skeletal muscle of male and female C57Bl6/6J and Sv/129 mice, and monoclonal and polyclonal cultures were treated with brown adipogenic medium. Additionally, FAPs were differentiated with medium supplemented or not with triiodothyronine. Results: Although skeletal muscle expression of uncoupling protein 1 (Ucp1) was barely detectable in uninjected tibialis anterior muscle, it was drastically induced following intramuscular adipogenesis in Sv/129 mice and further increased in response to beta 3-adrenergic stimulation. Intramuscular Ucp1 expression did not depend on IL-6 and was preserved in aged skeletal muscle. Myogenic progenitors did not form adipocytes neither in polyclonal nor monoclonal cultures. Fibro/adipogenic progenitors, on the other hand, readily differentiated into brown-like, UCP1 Conclusions: Intramuscular adipogenesis is associated with increased Ucp1 expression in skeletal muscle from obesity-resistant mice. Fibro/adipogenic progenitors provide a likely source for intramuscular adipocytes expressing UCP1 under control of both genetic and hormonal factors. Therefore, FAPs constitute a possible target for therapies aiming at the browning of intramuscular adipose tissue and the metabolic improvement of skeletal muscle affected by fatty infiltration.
MeSH term(s)	Adipocytes/metabolism ; Animals ; Female ; Humans ; Male ; Mice ; Muscle, Skeletal/metabolism ; Uncoupling Protein 1/metabolism
Chemical Substances	Uncoupling Protein 1
Language	English
Publishing date	2018-02-05
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.12277
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