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Article: Deletion of absent in melanoma (AIM) 2 gene alters bone morphology.

Gong, Zhenwei / Dixit, Manisha / Poudel, Sher Bahadur / Yildirim, Gozde / Yakar, Shoshanna / Muzumdar, Radhika

bioRxiv : the preprint server for biology

2024

Abstract: Absent in Melanoma (AIM) 2 is a gene that is induced by interferon and acts as a cytosolic sensor for double-stranded (ds) DNA. It forms the AIM2 inflammasome, leading to the production of interleukin (IL)-1β and IL-18. Our previous research demonstrated ...

Abstract	Absent in Melanoma (AIM) 2 is a gene that is induced by interferon and acts as a cytosolic sensor for double-stranded (ds) DNA. It forms the AIM2 inflammasome, leading to the production of interleukin (IL)-1β and IL-18. Our previous research demonstrated that mice lacking AIM2 exhibit spontaneous obesity, insulin resistance, and inflammation in adipose tissue. In this study, we aimed to explore the impact of AIM2 gene deletion on bone structure in adult and aged mice. Utilizing micro-computed tomography (micro-CT), we discovered that female mice lacking AIM2 showed an increase in the total cross-sectional area at 5 months of age, accompanied by an increase in cortical thickness in the mid-diaphysis of the femur at both 5 and 15 months of age. At 15 months of age, the cortical bone mineral density (BMD) significantly decreased in AIM2 null females compared to wild-type (WT) mice. In AIM2 null mice, both trabecular bone volume and BMD at the distal metaphysis of the femur significantly decreased at 5 and 15 months of age. Similarly, micro-CT analysis of the L4 vertebra revealed significant decreases in trabecular bone volume and BMD in aged AIM2 null females compared to WT mice. Histological examination of femurs from aged mice demonstrated increased bone marrow adiposity in AIM2 null mice, accompanied by a significant increase in CD45-/CD31-/Sca1+/Pdgfa+ adipose progenitor cells, and a decrease in the ratio of CD31-/CD31+ osteogenic progenitor cells, as determined by flow cytometry of bone marrow cells. Our findings suggest that AIM2 deficiency affects bone health by promoting adipogenesis in bone marrow cells and inducing a pro-inflammatory environment, potentially contributing to the decreased bone mineral density.
Language	English
Publishing date	2024-01-06
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.05.574199
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Article: Biopotentials of Collagen Scaffold Impregnated with Plant-Cell-Derived Epidermal Growth Factor in Defective Bone Healing.

Poudel, Sher Bahadur / Bhattarai, Govinda / Kwon, Tae-Ho / Lee, Jeong-Chae

Materials (Basel, Switzerland)

2023 Volume 16, Issue 9

Abstract: The combination of scaffolds with recombinant human epidermal growth factor (rhEGF) protein can enhance defective bone healing via synergistic activation to stimulate cellular growth, differentiation, and survival. We examined the biopotentials of an ... ...

Abstract	The combination of scaffolds with recombinant human epidermal growth factor (rhEGF) protein can enhance defective bone healing via synergistic activation to stimulate cellular growth, differentiation, and survival. We examined the biopotentials of an rhEGF-loaded absorbable collagen scaffold (ACS) using a mouse model of calvarial defects, in which the rhEGF was produced from a plant cell suspension culture system because of several systemic advantages. Here, we showed a successful and large-scale production of plant-cell-derived rhEGF protein (p-rhEGF) by introducing an expression vector that cloned with its cDNA under the control of rice α-amylase 3D promoter into rice calli (
Language	English
Publishing date	2023-04-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2487261-1
ISSN	1996-1944
ISSN	1996-1944
DOI	10.3390/ma16093335
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Article: Effects of GH/IGF axis on bone and cartilage

Dixit, Manisha / Poudel, Sher Bahadur / Yakar, Shoshana

Molecular and cellular endocrinology. 2021 Jan. 01, v. 519

2021

Abstract: Growth hormone (GH) and its mediator, the insulin-like growth factor-1 (IGF-1) regulate somatic growth, metabolism and many aspects of aging. As such, actions of GH/IGF have been studied in many tissues and organs over decades. GH and IGF-1 are part of ... ...

Abstract	Growth hormone (GH) and its mediator, the insulin-like growth factor-1 (IGF-1) regulate somatic growth, metabolism and many aspects of aging. As such, actions of GH/IGF have been studied in many tissues and organs over decades. GH and IGF-1 are part of the hypothalamic/pituitary somatotrophic axis that consists of many other regulatory hormones, receptors, binding proteins, and proteases. In humans, GH/IGF actions peak during pubertal growth and regulate skeletal acquisition through stimulation of extracellular matrix production and increases in bone mineral density. During aging the activity of these hormones declines, a state called somatopaguss, which associates with deleterious effects on the musculoskeletal system. In this review, we will focus on GH/IGF-1 action in bone and cartilage. We will cover many studies that have utilized congenital ablation or overexpression of members of this axis, as well as cell-specific gene-targeting approaches used to unravel the nature of the GH/IGF-1 actions in the skeleton in vivo.
Keywords	bone density ; cartilage ; extracellular matrix ; gene targeting ; insulin-like growth factor I ; metabolism ; proteinases ; skeleton ; somatotropin
Language	English
Dates of publication	2021-0101
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111052
Database	NAL-Catalogue (AGRICOLA)

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Article: Development of primary osteoarthritis during aging in genetically diverse UM-HET3 mice.

Poudel, Sher Bahadur / Ruff, Ryan R / Yildirim, Gozde / Miller, Richard A / Harrison, David E / Strong, Randy / Kirsch, Thorsten / Yakar, Shoshana

bioRxiv : the preprint server for biology

2024

Abstract: This study investigated the prevalence and progression of primary osteoarthritis (OA) in aged UM-HET3 mice. Using the Osteoarthritis Research Society International (OARSI) scoring system, we assessed articular cartilage (AC) integrity in 182 knee joints ... ...

Abstract	This study investigated the prevalence and progression of primary osteoarthritis (OA) in aged UM-HET3 mice. Using the Osteoarthritis Research Society International (OARSI) scoring system, we assessed articular cartilage (AC) integrity in 182 knee joints of 22-25 months old mice. Aged UM-HET3 mice showed a high prevalence of primary OA in both sexes. Significant positive correlations were found between cumulative AC (cAC) scores and synovitis in both sexes, and osteophyte formation in female mice. Ectopic chondrogenesis did not show significant correlations with cAC scores. Significant direct correlations were found between AC scores and inflammatory markers in chondrocytes, including matrix metalloproteinase-13 (MMP-13), inducible nitric oxide synthase (iNOS), and the NLR family pyrin domain containing-3 (NLRP3) inflammasome in both sexes, indicating a link between OA severity and inflammation. Additionally, markers of cell cycle arrest, such as p16 and β-galactosidase, also correlated with AC scores. Using micro-CT, we examined the correlations between subchondral bone (SCB) morphology traits and AC scores. In male mice, no significant correlations were found between SCB morphology traits and cAC scores, while in female mice, significant correlations were found between cAC scores and tibial SCB plate bone mineral density. Finally, we explored the effects of methylene blue (MB) and mitoquinone (MitoQ), two agents that affect mitochondrial function, on the prevalence and progression of OA during aging. Notably, MB and MitoQ treatments influenced the disease's progression in a sex-specific manner. MB treatment significantly reduced cAC scores at the medial knee joint, while MitoQ treatment reduced cAC scores, but these did not reach significance. In conclusion, our study provides comprehensive insights into the prevalence and progression of primary OA in aged UM-HET3 mice, highlighting the sex-specific effects of MB and MitoQ treatments. The correlations between AC scores and various pathological factors underscore the multifaceted nature of OA and its association with inflammation and subchondral bone changes.
Language	English
Publishing date	2024-01-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.16.571693
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Article: Development of primary osteoarthritis during aging in genetically diverse UM-HET3 mice.

Poudel, Sher Bahadur / Ruff, Ryan R / Yildirim, Gozde / Miller, Richard A / Harrison, David E / Strong, Randy / Kirsch, Thorsten / Yakar, Shoshana

Research square

2024

Abstract: Background: Primary osteoarthritis (OA) occurs without identifiable underlying causes such as previous injuries or specific medical conditions. Age is a major contributing factor to OA, and as one ages, various joint tissues undergo gradual change, ... ...

Abstract	Background: Primary osteoarthritis (OA) occurs without identifiable underlying causes such as previous injuries or specific medical conditions. Age is a major contributing factor to OA, and as one ages, various joint tissues undergo gradual change, including degeneration of the articular cartilage, alterations in subchondral bone (SCB) morphology, and inflammation of the synovium. Methods: We investigated the prevalence of primary OA in aged, genetically diverse UM-HET3 mice. Articular cartilage (AC) integrity and SCB morphology were assessed in 182 knee joints of 22-25 months old mice using the Osteoarthritis Research Society International (OARSI) scoring system and micro-CT, respectively. Additionally, we explored the effects of methylene blue (MB) and mitoquinone (MitoQ), two agents that affect mitochondrial function, on the prevalence and progression of OA during aging. Results: Aged UM-HET3 mice showed a high prevalence of primary OA in both sexes. Significant positive correlations were found between cumulative AC (cAC) scores and synovitis in both sexes, and osteophyte formation in female mice. Ectopic chondrogenesis did not show significant correlations with cAC scores. Significant direct correlations were found between AC scores and inflammatory markers in chondrocytes, including matrix metalloproteinase-13, inducible nitric oxide synthase, and the NLR family pyrin domain containing-3 inflammasome in both sexes, indicating a link between OA severity and inflammation. Additionally, markers of cell cycle arrest, such as p16 and β-galactosidase, also correlated with AC scores. In male mice, no significant correlations were found between SCB morphology traits and cAC scores, while in female mice, significant correlations were found between cAC scores and tibial SCB plate bone mineral density. Notably, MB and MitoQ treatments influenced the disease's progression in a sex-specific manner. MB treatment significantly reduced cAC scores at the medial knee joint, while MitoQ treatment reduced cAC scores, but these did not reach significance. Conclusions: Our study provides comprehensive insights into the prevalence and progression of primary OA in aged UM-HET3 mice, highlighting the sex-specific effects of MB and MitoQ treatments. The correlations between AC scores and various pathological factors underscore the multifaceted nature of OA and its association with inflammation and subchondral bone changes.
Language	English
Publishing date	2024-01-22
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3858256/v1
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Article ; Online: Effects of GH/IGF axis on bone and cartilage.

Dixit, Manisha / Poudel, Sher Bahadur / Yakar, Shoshana

Molecular and cellular endocrinology

2020 Volume 519, Page(s) 111052

Abstract	Growth hormone (GH) and its mediator, the insulin-like growth factor-1 (IGF-1) regulate somatic growth, metabolism and many aspects of aging. As such, actions of GH/IGF have been studied in many tissues and organs over decades. GH and IGF-1 are part of the hypothalamic/pituitary somatotrophic axis that consists of many other regulatory hormones, receptors, binding proteins, and proteases. In humans, GH/IGF actions peak during pubertal growth and regulate skeletal acquisition through stimulation of extracellular matrix production and increases in bone mineral density. During aging the activity of these hormones declines, a state called somatopaguss, which associates with deleterious effects on the musculoskeletal system. In this review, we will focus on GH/IGF-1 action in bone and cartilage. We will cover many studies that have utilized congenital ablation or overexpression of members of this axis, as well as cell-specific gene-targeting approaches used to unravel the nature of the GH/IGF-1 actions in the skeleton in vivo.
MeSH term(s)	Animals ; Bone Development ; Bone and Bones/metabolism ; Cartilage/metabolism ; Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/metabolism ; Osteoarthritis/metabolism ; Osteoarthritis/pathology
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6) ; Growth Hormone (9002-72-6)
Language	English
Publishing date	2020-10-14
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111052
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Article: Osteoblastic Wls Ablation Protects Mice from Total Body Irradiation-Induced Impairments in Hematopoiesis and Bone Marrow Microenvironment.

Sim, Hyun-Jaung / So, Han-Sol / Poudel, Sher Bahadur / Bhattarai, Govinda / Cho, Eui-Sic / Lee, Jeong-Chae / Kook, Sung-Ho

Aging and disease

2023 Volume 14, Issue 3, Page(s) 919–936

Abstract: Ionizing irradiation (IR) causes bone marrow (BM) injury, with senescence and impaired self-renewal of hematopoietic stem cells (HSCs), and inhibiting Wnt signaling could enhance hematopoietic regeneration and survival against IR stress. However, the ... ...

Abstract	Ionizing irradiation (IR) causes bone marrow (BM) injury, with senescence and impaired self-renewal of hematopoietic stem cells (HSCs), and inhibiting Wnt signaling could enhance hematopoietic regeneration and survival against IR stress. However, the underlying mechanisms by which a Wnt signaling blockade modulates IR-mediated damage of BM HSCs and mesenchymal stem cells (MSCs) are not yet completely understood. We investigated the effects of osteoblastic Wntless (Wls) depletion on total body irradiation (TBI, 5 Gy)-induced impairments in hematopoietic development, MSC function, and the BM microenvironment using conditional Wls knockout mutant mice (Col-Cre;Wls
Language	English
Publishing date	2023-06-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625789-0
ISSN	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2022.1026
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Article ; Online: Targeting mitochondrial dysfunction using methylene blue or mitoquinone to improve skeletal aging.

Poudel, Sher Bahadur / Frikha-Benayed, Dorra / Ruff, Ryan R / Yildirim, Gozde / Dixit, Manisha / Korstanje, Ron / Robinson, Laura / Miller, Richard A / Harrison, David E / Strong, John R / Schaffler, Mitchell B / Yakar, Shoshana

Aging

2024 Volume 16, Issue 6, Page(s) 4948–4964

Abstract: Methylene blue (MB) is a well-established antioxidant that has been shown to improve mitochondrial function in ... ...

Abstract	Methylene blue (MB) is a well-established antioxidant that has been shown to improve mitochondrial function in both
MeSH term(s)	Male ; Female ; Mice ; Animals ; Antioxidants/pharmacology ; Methylene Blue/pharmacology ; Mice, Inbred C57BL ; Oxidative Stress ; Aging ; Mitochondrial Diseases ; Organophosphorus Compounds ; Ubiquinone/analogs & derivatives
Chemical Substances	mitoquinone (47BYS17IY0) ; Antioxidants ; Methylene Blue (T42P99266K) ; Organophosphorus Compounds ; Ubiquinone (1339-63-5)
Language	English
Publishing date	2024-03-25
Publishing country	United States
Document type	Journal Article
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.205147
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Article ; Online: Local and Systemic Overexpression of COMP-Ang1 Induces Ang1/Tie2-Related Thrombocytopenia and SDF-1/CXCR4-Dependent Anemia.

Sim, Hyun-Jaung / Bhattarai, Govinda / Kim, Min-Hye / So, Han-Sol / Poudel, Sher Bahadur / Cho, Eui-Sic / Kook, Sung-Ho / Lee, Jeong-Chae

Stem cells (Dayton, Ohio)

2022 Volume 41, Issue 1, Page(s) 93–104

Abstract: While supplemental angiopoietin-1 (Ang1) improves hematopoiesis, excessive Ang1 induces bone marrow (BM) impairment, hematopoietic stem cell (HSC) senescence, and erythropoietic defect. Here, we examined how excessive Ang1 disturbs hematopoiesis and ... ...

Abstract	While supplemental angiopoietin-1 (Ang1) improves hematopoiesis, excessive Ang1 induces bone marrow (BM) impairment, hematopoietic stem cell (HSC) senescence, and erythropoietic defect. Here, we examined how excessive Ang1 disturbs hematopoiesis and explored whether hematopoietic defects were related to its level using K14-Cre;c-Ang1 and Col2.3-Cre;c-Ang1 transgenic mice that systemically and locally overexpress cartilage oligomeric matrix protein-Ang1, respectively. We also investigated the impacts of Tie2 inhibitor and AMD3100 on hematopoietic development. Transgenic mice exhibited excessive angiogenic phenotypes, but K14-Cre;c-Ang1 mice showed more severe defects in growth and life span with higher presence of Ang1 compared with Col2.3-Cre;c-Ang1 mice. Dissimilar to K14-Cre;c-Ang1 mice, Col2.3-Cre;c-Ang1 mice did not show impaired BM retention or senescence of HSCs, erythropoietic defect, or disruption of the stromal cell-derived factor 1 (SDF-1)/CXCR4 axis. However, these mice exhibited a defect in platelet production depending on the expression of Tie2 and globin transcription factor 1 (GATA-1), but not GATA-2, in megakaryocyte progenitor (MP) cells. Treatment with Tie2 inhibitor recovered GATA-1 expression in MP cells and platelet production without changes in circulating RBC in transgenic mice. Consecutive AMD3100 administration not only induced irrecoverable senescence of HSCs but also suppressed formation of RBC, but not platelets, via correlated decreases in number of erythroblasts and their GATA-1 expression in B6 mice. Our results indicate that genetic overexpression of Ang1 impairs hematopoietic development depending on its level, in which megakaryopoiesis is preferentially impaired via activation of Ang1/Tie2 signaling, whereas erythropoietic defect is orchestrated by HSC senescence, inflammation, and disruption of the SDF-1/CXCR4 axis.
MeSH term(s)	Mice ; Animals ; Cartilage Oligomeric Matrix Protein/genetics ; Angiopoietin-1/genetics ; Angiopoietin-1/metabolism ; Chemokine CXCL12/genetics ; Chemokine CXCL12/metabolism ; Mice, Transgenic ; Anemia/genetics ; Thrombocytopenia ; Receptor, TIE-2/genetics ; Receptor, TIE-2/metabolism
Chemical Substances	plerixafor (S915P5499N) ; Cartilage Oligomeric Matrix Protein ; Angiopoietin-1 ; Chemokine CXCL12 ; Receptor, TIE-2 (EC 2.7.10.1)
Language	English
Publishing date	2022-11-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1093/stmcls/sxac080
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Article ; Online: Anti-inflammatory, anti-osteoclastic, and antioxidant activities of genistein protect against alveolar bone loss and periodontal tissue degradation in a mouse model of periodontitis.

Bhattarai, Govinda / Poudel, Sher Bahadur / Kook, Sung-Ho / Lee, Jeong-Chae

Journal of biomedical materials research. Part A

2017 Volume 105, Issue 9, Page(s) 2510–2521

Abstract: Genistein, a dietary polyphenol primarily found in soy products, has beneficial effects on bone. However, the effect of genistein on inflammatory periodontal destruction has not been investigated in detail. We explored whether genistein protects against ... ...

Abstract	Genistein, a dietary polyphenol primarily found in soy products, has beneficial effects on bone. However, the effect of genistein on inflammatory periodontal destruction has not been investigated in detail. We explored whether genistein protects against lipopolysaccharide (LPS)/ligature-induced periodontitis in mice. We also examined the effect of genistein on LPS-stimulated inflammatory and oxidative stress using RAW 264.7 macrophages and human gingival fibroblasts (hGFs). The results from μCT and histological analyses revealed that intraperitoneal injection of genistein (20 mg/kg body weight) daily for three weeks inhibited LPS-mediated alveolar bone loss and periodontal tissue degradation. The administration of genistein also inhibited osteoclast formation and the expression of inflammation-related molecules in the inflamed region of mice with periodontitis. Treatment with 30-70 μM genistein significantly prevented osteoclast differentiation in receptor activator of nuclear factor κB ligand- or LPS-stimulated macrophages by suppressing the expression of osteoclast-specific molecules. The addition of genistein led to a dose-dependent inhibition of the expression of inflammation-related molecules both in LPS-stimulated macrophages and hGFs. In addition, genistein at 50 μM protected hGFs from LPS-mediated stresses such as mitochondrial impairment and cellular ROS accumulation. However, such protection was significantly diminished by combined treatment with 25 nM bafilomycin A1, a chemical autophagy inhibitor. Collectively, our results indicate that genistein protects against inflammatory periodontal damage by regulating autophagy induction and inhibiting osteoclast activation, the production of inflammation mediators, and mitochondrial oxidative damage. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2510-2521, 2017.
Language	English
Publishing date	2017-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2099989-6
ISSN	1552-4965 ; 1549-3296 ; 0021-9304
ISSN (online)	1552-4965
ISSN	1549-3296 ; 0021-9304
DOI	10.1002/jbm.a.36109
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