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Article ; Online: Role of Klotho in bone and implication for CKD.

Komaba, Hirotaka / Lanske, Beate

Current opinion in nephrology and hypertension

2018 Volume 27, Issue 4, Page(s) 298–304

Abstract: Purpose of review: Klotho is a transmembrane protein that acts as a co-receptor for fibroblast growth factor 23 (FGF23). Recent investigations have discovered the presence of Klotho in bone-forming osteoblasts and osteocytes. This review summarizes ... ...

Abstract	Purpose of review: Klotho is a transmembrane protein that acts as a co-receptor for fibroblast growth factor 23 (FGF23). Recent investigations have discovered the presence of Klotho in bone-forming osteoblasts and osteocytes. This review summarizes emerging literature on the roles of bone Klotho in mineral and bone metabolism and discusses their possible involvement in renal osteodystrophy. Recent findings: Mouse genetic studies have demonstrated that loss of Klotho in osteocytes leads to increased bone formation and bone volume. The identification of Klotho expression in bone cells pointed to the possibility that the bone is another target organ for FGF23, providing a new basis for extending the interpretation of previous research findings. Along with this paradigm shift, recent investigations uncovered the autocrine/paracrine functions of FGF23 as a critical regulator of its own production and the Wnt-mediated bone formation. These effects may, however, be offset by down-regulation of bone Klotho in renal failure. Summary: Klotho expressed in bone cells has functional roles in controlling bone formation and regulating FGF23 production. Additional studies are needed to translate these findings into the development of new therapeutic approaches for the treatment of bone fragility in patients with renal osteodystrophy and other bone diseases.
MeSH term(s)	Animals ; Bone and Bones/cytology ; Bone and Bones/metabolism ; Chronic Kidney Disease-Mineral and Bone Disorder/metabolism ; Down-Regulation ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Humans ; Osteocytes/metabolism ; Renal Insufficiency, Chronic/metabolism ; Wnt Proteins/metabolism
Chemical Substances	Wnt Proteins ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2018-04-25
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000423
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Article ; Online: Biology of Fibroblast Growth Factor 23: From Physiology to Pathology.

Courbebaisse, Marie / Lanske, Beate

Cold Spring Harbor perspectives in medicine

2018 Volume 8, Issue 5

Abstract: Fibroblast growth factor (FGF)23 is a phosphaturic hormone produced by osteocytes and osteoblasts that binds to FGF receptors in the presence of the transmembrane protein αKlotho. FGF23 mainly targets the renal proximal tubule to inhibit calcitriol ... ...

Abstract	Fibroblast growth factor (FGF)23 is a phosphaturic hormone produced by osteocytes and osteoblasts that binds to FGF receptors in the presence of the transmembrane protein αKlotho. FGF23 mainly targets the renal proximal tubule to inhibit calcitriol production and the expression of the sodium/phosphate cotransporters NaPi2a and NaPi2c, thus inhibiting renal phosphate reabsorption. FGF23 also acts on the parathyroid glands to inhibit parathyroid hormone synthesis and secretion. FGF23 regulation involves many systemic and local factors, among them calcitriol, phosphate, and parathyroid hormone. Increased FGF23 is primarily observed in rare acquired or genetic disorders, but chronic kidney disease is associated with a reactional increase in FGF23 to combat hyperphosphatemia. However, high FGF23 levels induce left ventricular hypertrophy (LVH) and are associated with an increased risk of mortality. In this review, we describe FGF23 physiology and the pathological consequences of high or low FGF23 levels.
MeSH term(s)	Bone and Bones/metabolism ; Calcitriol/metabolism ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/physiology ; Humans ; Hypertrophy, Left Ventricular/metabolism ; Phosphates/metabolism ; Renal Reabsorption/physiology
Chemical Substances	FGF23 protein, human ; Phosphates ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Calcitriol (FXC9231JVH)
Language	English
Publishing date	2018-05-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a031260
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Article: Parathyroid Hormone-Related Peptide and Its Analog, Abaloparatide, Attenuate Lethal Myocardial Ischemia-Reperfusion Injury.

Wider, Joseph / Undyala, Vishnu V R / Lanske, Beate / Datta, Nabanita S / Przyklenk, Karin

Journal of clinical medicine

2022 Volume 11, Issue 9

Abstract: Parathyroid hormone-related peptide (PTHrP) is well-known to play a role in bone formation, and abaloparatide, an analog of PTHrP(1-34), is approved for the treatment of osteoporosis in post-menopausal women. PTHrP has also been reported to have ... ...

Abstract	Parathyroid hormone-related peptide (PTHrP) is well-known to play a role in bone formation, and abaloparatide, an analog of PTHrP(1-34), is approved for the treatment of osteoporosis in post-menopausal women. PTHrP has also been reported to have cardiovascular effects, with recent data demonstrating that exogenously administered PTHrP can limit the death of isolated cardiomyocytes subjected to oxidative stress via upregulation of classic ‘survival kinase’ signaling. Our aim in the current study was to extend this concept and, employing both in vitro and in vivo models, establish whether PTHrP(1-36) and abaloparatide are cardioprotective in the setting of lethal myocardial ischemia-reperfusion injury. We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059. Moreover, using the translationally relevant swine model of acute coronary artery occlusion-reperfusion, we make the novel observation that myocardial infarct size was significantly reduced in pigs pretreated with PTHrP(1-36) when compared with placebo-controls (13.1 ± 3.3% versus 42.0 ± 6.6% of the area of at-risk myocardium, respectively; p < 0.01). Taken together, these data provide the first evidence in support of the concept that pretreatment with PTHrP(1-36) and abaloparatide renders cardiomyocytes resistant to lethal myocardial ischemia-reperfusion injury.
Language	English
Publishing date	2022-04-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm11092273
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Article ; Online: Bone Marrow Adipose Tissue: The First 40 Years.

Lanske, Beate / Rosen, Clifford

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2017 Volume 32, Issue 6, Page(s) 1153–1156

MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue/physiology ; Adiposity ; Animals ; Bone Marrow/physiology ; Humans ; Phenotype ; X-Ray Microtomography
Language	English
Publishing date	2017-04-14
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.3140
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Article ; Online: Parathyroid Hormone-Related Peptide and Its Analog, Abaloparatide, Attenuate Lethal Myocardial Ischemia-Reperfusion Injury

Joseph Wider / Vishnu V. R. Undyala / Beate Lanske / Nabanita S. Datta / Karin Przyklenk

Journal of Clinical Medicine, Vol 11, Iss 2273, p

2022 Volume 2273

Abstract	Parathyroid hormone-related peptide (PTHrP) is well-known to play a role in bone formation, and abaloparatide, an analog of PTHrP(1-34), is approved for the treatment of osteoporosis in post-menopausal women. PTHrP has also been reported to have cardiovascular effects, with recent data demonstrating that exogenously administered PTHrP can limit the death of isolated cardiomyocytes subjected to oxidative stress via upregulation of classic ‘survival kinase’ signaling. Our aim in the current study was to extend this concept and, employing both in vitro and in vivo models, establish whether PTHrP(1-36) and abaloparatide are cardioprotective in the setting of lethal myocardial ischemia-reperfusion injury. We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059. Moreover, using the translationally relevant swine model of acute coronary artery occlusion-reperfusion, we make the novel observation that myocardial infarct size was significantly reduced in pigs pretreated with PTHrP(1-36) when compared with placebo-controls (13.1 ± 3.3% versus 42.0 ± 6.6% of the area of at-risk myocardium, respectively; p < 0.01). Taken together, these data provide the first evidence in support of the concept that pretreatment with PTHrP(1-36) and abaloparatide renders cardiomyocytes resistant to lethal myocardial ischemia-reperfusion injury.
Keywords	myocardial ischemia ; myocardial infarction ; infarct size ; ischemia-reperfusion injury ; cardioprotection ; parathyroid hormone-related peptide ; Medicine ; R
Subject code	610
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Comparative study in estrogen-depleted mice identifies skeletal and osteocyte transcriptomic responses to abaloparatide and teriparatide.

Lv, Zhengtao / Zhang, Jiaming / Liang, Shuang / Zhou, Chenhe / Hu, Dorothy / Brooks, Daniel J / Bouxsein, Mary L / Lanske, Beate / Kostenuik, Paul / Gori, Francesca / Baron, Roland

JCI insight

2023 Volume 8, Issue 20

Abstract: Osteocytes express parathyroid hormone (PTH)/PTH-related protein (PTHrP) receptors and respond to the PTHrP analog abaloparatide (ABL) and to the PTH 1-34 fragment teriparatide (TPTD), which are used to treat osteoporosis. Several studies indicate ... ...

Abstract	Osteocytes express parathyroid hormone (PTH)/PTH-related protein (PTHrP) receptors and respond to the PTHrP analog abaloparatide (ABL) and to the PTH 1-34 fragment teriparatide (TPTD), which are used to treat osteoporosis. Several studies indicate overlapping but distinct skeletal responses to ABL or TPTD, but their effects on cortical bone may differ. Little is known about their differential effects on osteocytes. We compared cortical osteocyte and skeletal responses to ABL and TPTD in sham-operated and ovariectomized mice. Administered 7 weeks after ovariectomy for 4 weeks at a dose of 40 μg/kg/d, TPTD and ABL had similar effects on trabecular bone, but ABL showed stronger effects in cortical bone. In cortical osteocytes, both treatments decreased lacunar area, reflecting altered peri-lacunar remodeling favoring matrix accumulation. Osteocyte RNA-Seq revealed that several genes and pathways were altered by ovariectomy and affected similarly by TPTD and ABL. Notwithstanding, several signaling pathways were uniquely regulated by ABL. Thus, in mice, TPTD and ABL induced a positive osteocyte peri-lacunar remodeling balance, but ABL induced stronger cortical responses and affected the osteocyte transcriptome differently. We concluded that ABL affected the cortical osteocyte transcriptome in a manner subtly different from TPTD, resulting in more beneficial remodeling/modeling changes and homeostasis of the cortex.
MeSH term(s)	Female ; Mice ; Animals ; Teriparatide/pharmacology ; Teriparatide/therapeutic use ; Parathyroid Hormone-Related Protein/pharmacology ; Parathyroid Hormone-Related Protein/metabolism ; Osteocytes/metabolism ; Transcriptome ; Estrogens/pharmacology
Chemical Substances	Teriparatide (10T9CSU89I) ; abaloparatide (AVK0I6HY2U) ; Parathyroid Hormone-Related Protein ; Estrogens
Language	English
Publishing date	2023-10-23
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.161932
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Article ; Online: Crosstalk between kidney and bone - Bench to bedside.

Hruska, Keith A / Lanske, Beate / Moe, Orson W

Bone

2017 Volume 100, Page(s) 1–3

MeSH term(s)	Animals ; Bone and Bones/physiology ; Disease Models, Animal ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/metabolism ; Glucuronidase/metabolism ; Humans ; Kidney/physiology ; Klotho Proteins ; Mice ; Signal Transduction ; Translational Research, Biomedical
Chemical Substances	Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2017-04-11
Publishing country	United States
Document type	Editorial ; Introductory Journal Article
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2017.03.046
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Effects of systemically administered abaloparatide, an osteoanabolic PTHrP analog, as an adjuvant therapy for spinal fusion in rats.

Arlt, Heike / Besschetnova, Tatiana / Ominsky, Michael S / Fredericks, Douglas C / Lanske, Beate

JOR spine

2020 Volume 4, Issue 1, Page(s) e1132

Abstract: Background: Abaloparatide is a parathyroid hormone receptor agonist that increases bone formation and reduces vertebral and nonvertebral fracture risk in women with postmenopausal osteoporosis. Animal studies indicate abaloparatide stimulates vertebral ... ...

Abstract	Background: Abaloparatide is a parathyroid hormone receptor agonist that increases bone formation and reduces vertebral and nonvertebral fracture risk in women with postmenopausal osteoporosis. Animal studies indicate abaloparatide stimulates vertebral bone formation and enhances bony bridging and biomechanical stability of fracture calluses. Aims: The current study is evaluating the potential utility for abaloparatide as an adjunct therapy for spinal fusions. Material and methods: The effects of 14 or 28 days of daily subcutaneous injections of abaloparatide (20 μg/kg/d) or vehicle were evaluated in 32 male Sprague-Dawley rats starting 1 day after noninstrumented posterolateral fusion (PLF) with bone autograft. Fusion mass microarchitecture was analyzed by micro-computed tomography (micro-CT) and serum markers of bone formation and bone resorption were evaluated. Motion segments were scored in a blinded manner as fused or unfused by postmortem radiography and manual palpation. Results: Abaloparatide-treated rats showed higher bone formation (serum osteocalcin) at day 14 and 28 compared with vehicle controls, without increases in the bone resorption marker serum TRACP-5b. Micro-CT showed greater trabecular number in fusion masses from the abaloparatide group vs vehicle controls at day 14. Manual palpation and radiography indicated no fusions in either group at day 14, whereas 25% of vehicle-treated rats and 50% of abaloparatide-treated rats had bilateral fusion at day 28. Discussion and conclusion: In summary, this rat PLF model showed that abaloparatide treatment was associated with higher levels of the bone formation marker osteocalcin, improved fusion mass architecture, and a non- significant 2-fold higher fusion rate compared with vehicle.
Language	English
Publishing date	2020-11-25
Publishing country	United States
Document type	Journal Article
ISSN	2572-1143
ISSN (online)	2572-1143
DOI	10.1002/jsp2.1132
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Article ; Online: Molecular interactions of FGF23 and PTH in phosphate regulation.

Lanske, Beate / Razzaque, Mohammed S

Kidney international

2014 Volume 86, Issue 6, Page(s) 1072–1074

Abstract: Bone-derived fibroblast growth factor-23 (FGF23) plays an important role in systemic phosphate turnover. Increased FGF23 activity results in hypophosphatemic disorders, while reduced activity is linked to hyperphosphatemic disorders. FGF23, together with ...

Abstract	Bone-derived fibroblast growth factor-23 (FGF23) plays an important role in systemic phosphate turnover. Increased FGF23 activity results in hypophosphatemic disorders, while reduced activity is linked to hyperphosphatemic disorders. FGF23, together with klotho as co-factor, can activate FGF receptors in its target tissues to exert its functions. However, the molecular regulation of FGF23 synthesis is not clearly defined, and recent studies have found that parathyroid hormone (PTH) can activate the nuclear receptor-associated protein-1 (Nurr1) to induce FGF23 transcription in bone cells.
MeSH term(s)	Animals ; Fibroblast Growth Factors/genetics ; Male ; Nuclear Receptor Subfamily 4, Group A, Member 2/genetics ; Nuclear Receptor Subfamily 4, Group A, Member 2/metabolism ; Parathyroid Hormone/pharmacology ; RNA, Messenger/metabolism ; Transcription, Genetic/drug effects
Chemical Substances	Nuclear Receptor Subfamily 4, Group A, Member 2 ; Parathyroid Hormone ; RNA, Messenger ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2014-12
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2014.316
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Zs.A 797: Show issues

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Article ; Online: Effects of klotho deletion from bone during chronic kidney disease.

Kaludjerovic, Jovana / Komaba, Hirotaka / Lanske, Beate

Bone

2017 Volume 100, Page(s) 50–55

Abstract: Klotho is a type I transmembrane protein that acts as a permissive co-receptor for FGF23 and helps to maintain proper mineral metabolism. Mice carrying a loss-of-function mutation in either the Klotho or Fgf23 gene develop many similar phenotypes ... ...

Abstract	Klotho is a type I transmembrane protein that acts as a permissive co-receptor for FGF23 and helps to maintain proper mineral metabolism. Mice carrying a loss-of-function mutation in either the Klotho or Fgf23 gene develop many similar phenotypes including osteoporosis. Based on these observations it was hypothesized that the bone phenotypes in Klotho- and Fgf23-null mice may be mediated through a common signaling pathway. Recent improvements in antibody specificity have shown that osteoblasts and osteocytes, which produce FGF23, also express low amount of membrane Klotho. But, the role of Klotho in bone is still largely unclear. In this review we summarize the literature and show that Klotho has an FGF23 dependent and independent effect in bone.
MeSH term(s)	Animals ; Bone and Bones/metabolism ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Humans ; Klotho Proteins ; Osteoblasts/metabolism ; Osteocytes/metabolism ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction ; Vitamin D/metabolism
Chemical Substances	FGF23 protein, human ; Fgf23 protein, mouse ; Vitamin D (1406-16-2) ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2017-02-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2017.02.006
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