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Article ; Online: Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2.

Riggs, Keegan C / Sankar, Uma

Immunometabolism (Cobham, Surrey)

2023 Volume 5, Issue 4, Page(s) e00031

Abstract: Post-traumatic osteoarthritis (PTOA) is a multifactorial disease of the cartilage, synovium, and subchondral bone resulting from direct joint trauma and altered joint mechanics after traumatic injury. There are no current disease-modifying therapies for ... ...

Abstract	Post-traumatic osteoarthritis (PTOA) is a multifactorial disease of the cartilage, synovium, and subchondral bone resulting from direct joint trauma and altered joint mechanics after traumatic injury. There are no current disease-modifying therapies for PTOA, and early surgical interventions focused on stabilizing the joint do not halt disease progression. Chronic pain and functional disability negatively affect the quality of life and take an economic toll on affected patients. While multiple mechanisms are at play in disease progression, joint inflammation is a key contributor. Impact-induced mitochondrial dysfunction and cell death or altered joint mechanics after trauma culminate in inflammatory cytokine release from synoviocytes and chondrocytes, cartilage catabolism, suppression of cartilage anabolism, synovitis, and subchondral bone disease, highlighting the complexity of the disease. Current understanding of the cellular and molecular mechanisms underlying the disease pathology has allowed for the investigation of a variety of therapeutic strategies that target unique apoptotic and/or inflammatory processes in the joint. This review provides a concise overview of the inflammatory and apoptotic mechanisms underlying PTOA pathogenesis and identifies potential therapeutic targets to mitigate disease progression. We highlight Ca
Language	English
Publishing date	2023-10-16
Publishing country	England
Document type	Journal Article ; Review
ISSN	2633-0407
ISSN (online)	2633-0407
DOI	10.1097/IN9.0000000000000031
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Article: Editorial: Bone inside-out and outside-in signals: Control of body homeostasis.

Sankar, Uma / Brun, Lucas R / Plotkin, Lilian I

Frontiers in endocrinology

2023 Volume 13, Page(s) 1120215

MeSH term(s)	Bone and Bones ; Osteoblasts ; Homeostasis
Language	English
Publishing date	2023-01-06
Publishing country	Switzerland
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2022.1120215
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Article ; Online: Conditional loss of CaMKK2 in Osterix-positive osteoprogenitors enhances osteoblast function in a sex-divergent manner.

Mattingly, Brett T / Kambrath, Anuradha Valiya / Ding, Xinchun / Thompson, William R / Sankar, Uma

Bone

2024 Volume 184, Page(s) 117113

Abstract: ... ...

Abstract	Ca
MeSH term(s)	Animals ; Osteoblasts/metabolism ; Female ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Male ; Sp7 Transcription Factor/metabolism ; Sp7 Transcription Factor/genetics ; Osteogenesis/physiology ; Sex Characteristics ; Mice ; Mice, Knockout ; Osteoclasts/metabolism ; Stem Cells/metabolism ; Gene Deletion
Chemical Substances	Camkk2 protein, mouse ; Sp7 protein, mouse
Language	English
Publishing date	2024-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2024.117113
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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)
Zs.MO 332: Show issues

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Article: Post-traumatic osteoarthritis: A review of pathogenic mechanisms and novel targets for mitigation.

Dilley, Julian E / Bello, Margaret Anne / Roman, Natoli / McKinley, Todd / Sankar, Uma

Bone reports

2023 Volume 18, Page(s) 101658

Abstract: Post-traumatic osteoarthritis (PTOA) develops secondary to a joint injury and accounts for 12 % of all osteoarthritis. These injuries, often of the lower extremity joints, occur due to trauma or accidents related to athletic or military activities. They ... ...

Abstract	Post-traumatic osteoarthritis (PTOA) develops secondary to a joint injury and accounts for 12 % of all osteoarthritis. These injuries, often of the lower extremity joints, occur due to trauma or accidents related to athletic or military activities. They primarily affect younger individuals although PTOA can occur across the spectrum of age. Pain and functional disability caused by PTOA confer a heavy economic toll on patients, in addition to detrimentally affecting their quality of life. Both high energy injuries that cause articular surface fracture with or without subchondral bone disruption and low-energy injuries involving joint dislocations or ligamentous injury cause PTOA, albeit through different mechanisms. Regardless, chondrocyte death, mitochondrial dysfunction, reactive oxygen species production, subchondral bone remodeling, inflammation and cytokine release in the cartilage and synovium play integral roles in the pathogenesis of PTOA. Evolving surgical methods are focused on stabilizing articular surface and joint structure congruity. However, to date there are no disease modifying medical therapies against PTOA. Increased recent understanding of the pathogenesis of the subchondral bone and synovial inflammation as well as that of chondrocyte mitochondrial dysfunction and apoptosis have led to the investigation of new therapeutics targeting these mechanisms to prevent or delay PTOA. This review discusses new advances in our understanding of cellular mechanisms underlying PTOA, and therapeutic approaches that are potentially effective in reducing the self-propagating cycle of subchondral bone alterations, inflammation, and cartilage degradation. Within this context, we focus therapeutic options involving anti-inflammatory and anti-apoptotic candidates that could prevent PTOA.
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821774-3
ISSN	2352-1872
ISSN	2352-1872
DOI	10.1016/j.bonr.2023.101658
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Article ; Online: CaMKK2 Signaling in Metabolism and Skeletal Disease: a New Axis with Therapeutic Potential.

Williams, Justin N / Sankar, Uma

Current osteoporosis reports

2019 Volume 17, Issue 4, Page(s) 169–177

Abstract: Purpose of review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to ... ...

Abstract	Purpose of review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to fractures and its regenerative capacity diminishes under such conditions. With a rapidly aging population in the USA and the global increase in diabetes, efficacious, multi-dimensional therapies that can treat or prevent skeletal diseases associated with metabolic dysfunction and inflammatory disorders are acutely needed. Recent findings: Ca
MeSH term(s)	Aging/metabolism ; Bone Diseases, Metabolic/etiology ; Bone Diseases, Metabolic/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Energy Metabolism ; Fracture Healing ; Glycation End Products, Advanced/metabolism ; Humans ; Inflammation/metabolism ; Obesity/metabolism
Chemical Substances	Glycation End Products, Advanced ; CAMKK2 protein, human (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17)
Language	English
Publishing date	2019-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-019-00518-w
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Zs.A 6146: Show issues

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Article ; Online: An Improved Methodology to Evaluate Cell and Molecular Signals in the Reparative Callus During Fracture Healing.

Valiya Kambrath, Anuradha / Williams, Justin N / Sankar, Uma

The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society

2020 Volume 68, Issue 3, Page(s) 199–208

Abstract: Approximately 5% to 10% of all bone fractures do not heal completely, contributing to significant patient suffering and medical costs. Even in healthy individuals, fracture healing is associated with significant downtime and loss of productivity. However, ...

Abstract	Approximately 5% to 10% of all bone fractures do not heal completely, contributing to significant patient suffering and medical costs. Even in healthy individuals, fracture healing is associated with significant downtime and loss of productivity. However, no pharmacological treatments are currently available to promote efficient bone healing. A better understanding of the underlying molecular mechanisms is crucial for developing novel therapies to hasten healing. The early reparative callus that forms around the site of bone injury is a fragile tissue consisting of shifting cell populations held together by loose connective tissue. The delicate callus is challenging to section and is vulnerable to disintegration during the harsh steps of immunostaining, namely, decalcification, deparaffinization, and antigen retrieval. Here, we describe an improved methodology for processing early-stage fracture calluses and immunofluorescence labeling of the sections to visualize the temporal (timing) and spatial (location) patterns of cellular and molecular events that regulate bone healing. This method has a short turnaround time from sample collection to microscopy as it does not require lengthy decalcification. It preserves the structural integrity of the fragile callus as the method does not entail deparaffinization or harsh methods of antigen retrieval. Our method can be adapted for high-throughput screening of drugs that promote efficacious bone healing.
MeSH term(s)	Animals ; Bone Development/physiology ; Bony Callus/metabolism ; Cartilage/metabolism ; Cell Differentiation ; Cell Proliferation ; Femur/metabolism ; Fluorescent Dyes/chemistry ; Fracture Healing/physiology ; Male ; Mice, Inbred C57BL ; Optical Imaging/methods ; Osteoblasts/metabolism ; Phenazines/metabolism ; Signal Transduction ; Time Factors
Chemical Substances	Fluorescent Dyes ; Phenazines ; safranine T (XTX0YXU2HV)
Language	English
Publishing date	2020-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	218208-7
ISSN	1551-5044 ; 0022-1554
ISSN (online)	1551-5044
ISSN	0022-1554
DOI	10.1369/0022155419900915
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Article ; Online: CaMKK2 Knockout Bone Marrow Cells Collected/Processed in Low Oxygen (Physioxia) Suggests CaMKK2 as a Hematopoietic Stem to Progenitor Differentiation Fate Determinant.

Broxmeyer, Hal E / Ropa, James / Capitano, Maegan L / Cooper, Scott / Racioppi, Luigi / Sankar, Uma

Stem cell reviews and reports

2022 Volume 18, Issue 7, Page(s) 2513–2521

Abstract: Little is known about a regulatory role of CaMKK2 for hematopoietic stem (HSC) and progenitor (HPC) cell function. To assess this, we used Camkk2-/- and wild type (WT) control mouse bone marrow (BM) cells. BM cells were collected/processed and compared ... ...

Abstract	Little is known about a regulatory role of CaMKK2 for hematopoietic stem (HSC) and progenitor (HPC) cell function. To assess this, we used Camkk2-/- and wild type (WT) control mouse bone marrow (BM) cells. BM cells were collected/processed and compared under hypoxia (3% oxygen; physioxia) vs. ambient air (~21% oxygen). Subjecting cells collected to ambient air, even for a few minutes, causes a stress that we termed Extra Physiological Shock/Stress (EPHOSS) that causes differentiation of HSCs and HPCs. We consider physioxia collection/processing a more relevant way to assess HSC/HPC numbers and function, as the cells remain in an oxygen tension closer physiologic conditions. Camkk2-/- cells collected/processed at 3% oxygen had positive and negative effects respectively on HSCs (by engraftment using competitive transplantation with congenic donor and competitor cells and lethally irradiated congenic recipient mice), and HPCs (by colony forming assays of CFU-GM, BFU-E, and CFU-GEMM) compared to WT cells processed in ambient air. Thus, with cells collected/processed under physioxia, and therefore never exposed and naïve to ambient air conditions, CaMKK2 not only appears to act as an HSC to HPC differentiation fate determinant, but as we found for other intracellular mediators, the Camkk-/- mouse BM cells were relatively resistant to effects of EPHOSS. This information is of potential use for modulation of WT BM HSCs and HPCs for future clinical advantage.
MeSH term(s)	Animals ; Bone Marrow Cells ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/genetics ; Hematopoietic Stem Cell Transplantation ; Mice ; Mice, Knockout ; Oxygen/pharmacology
Chemical Substances	Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17) ; Camkk2 protein, mouse (EC 2.7.11.17) ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2495577-2
ISSN	2629-3277 ; 1558-6804 ; 1550-8943
ISSN (online)	2629-3277 ; 1558-6804
ISSN	1550-8943
DOI	10.1007/s12015-021-10306-8
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Zs.A 6198: Show issues

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Article ; Online: Decreased SIRT1 Activity Is Involved in the Acute Injury Response of Chondrocytes to Ex Vivo Injurious Mechanical Overload.

Karnik, Sonali / Noori-Dokht, Hessam / Williams, Taylor / Joukar, Amin / Trippel, Stephen B / Sankar, Uma / Wagner, Diane R

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: A better understanding of molecular events following cartilage injury is required to develop treatments that prevent or delay the onset of trauma-induced osteoarthritis. In this study, alterations to SIRT1 activity in bovine articular cartilage explants ... ...

Abstract	A better understanding of molecular events following cartilage injury is required to develop treatments that prevent or delay the onset of trauma-induced osteoarthritis. In this study, alterations to SIRT1 activity in bovine articular cartilage explants were evaluated in the 24 h following a mechanical overload, and the effect of pharmacological SIRT1 activator SRT1720 on acute chondrocyte injury was assessed. SIRT1 enzymatic activity decreased as early as 5 min following the mechanical overload, and remained suppressed for at least 24 h. The chondrocyte injury response, including apoptosis, oxidative stress, secretion of inflammatory mediators, and alterations in cartilage matrix expression, was prevented with pharmacological activation of SIRT1 in a dose-dependent manner. Overall, the results implicate SIRT1 deactivation as a key molecular event in chondrocyte injury following a mechanical impact overload. As decreased SIRT1 signaling is associated with advanced age, these findings suggest that downregulated SIRT1 activity may be common to both age-related and injury-induced osteoarthritis.
MeSH term(s)	Animals ; Cattle ; Chondrocytes/metabolism ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; Cartilage, Articular/metabolism ; Apoptosis ; Osteoarthritis/etiology ; Osteoarthritis/metabolism ; Musculoskeletal Diseases/metabolism
Chemical Substances	Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2023-03-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076521
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Article: Measuring childhood socioeconomic position in health research: Development and validation of childhood socioeconomic position questionnaire using mixed method approach.

Sankar, Uma Vadassery / Kutty, V Raman / Anand, T N

Health promotion perspectives

2019 Volume 9, Issue 1, Page(s) 40–49

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2019-01-23
Publishing country	Iran
Document type	Journal Article
ZDB-ID	2691688-5
ISSN	2228-6497
ISSN	2228-6497
DOI	10.15171/hpp.2019.05
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Article ; Online: High prevalence of "non-pathogenic" POLE mutation with poor prognosis in a cohort of endometrial cancer from South India.

Kuriakose, Santhosh / Dhanasooraj, Dhananjayan / Shiny, P M / Shammy, S / Sona, V P / Manjula, Anupama A / Ramachandran, Amrutha / Vijaykumar, Bindu / Susan, Nayana / Dinesan, M / Sankar, Uma V / Ramachandran, Kavitha / Sreedharan, P S

International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics

2024

Abstract: Objective: The Cancer Genome Atlas (TCGA) project identified favorable prognosis regarding the ultra-mutated endometrial cancer (EC) subtype linked to polymerase epsilon gene (POLE) mutations. This study investigated POLE mutations in EC of Indian ... ...

Abstract	Objective: The Cancer Genome Atlas (TCGA) project identified favorable prognosis regarding the ultra-mutated endometrial cancer (EC) subtype linked to polymerase epsilon gene (POLE) mutations. This study investigated POLE mutations in EC of Indian patients. Methods: This retrospective analytical study was conducted between January 2016 and January 2023 at the Government Medical College, Kozhikode, and the MVR Cancer Center, Kozhikode, Kerala. Sanger sequencing of POLE gene exons 9 and 13 in 151 EC patients was carried out to analyze the relationship between mutations and epidemiological factors, clinicopathologic features, and treatment outcomes. Results: Among 151 cases enrolled, 39 were unique POLE-mutated cases. Significant associations were high-grade tumors, myometrial invasion >50%, and Lymph-vascular space invasion (LVSI). The median follow-up was 40 months (95% confidence interval [CI], 34-46). A lower mean disease-specific survival (DSS) of 51.7 months (95% CI, 43.7-59.6) was noted in the POLE-mutated group compared with 72.11 months (95% CI, 67.60-76.62) for the POLE wild-type. A statistically significant hazard ratio (HR) of 2.683 for DSS in the POLE-mutated group was noted. In advanced stages (FIGO stages II-IV), a nine-fold HR for DSS and overall survival (OS) compared with POLE wild-type was identified. After controlling for treatment effects using Cox proportional HR, advanced-stage POLE-mutated tumors had a significantly higher HR of 8.67 for DSS compared with POLE-wild-type tumors of the same stage. Conclusion: This study identified a unique set of POLE mutations in Indian EC patients associated with poor prognosis, which were particularly pronounced in advanced stages. Advanced stage of presentation, type of POLE mutations, and possibly ethnicity are predictors of adverse outcomes in POLE-mutated EC. The present study highlights ethnicity as a determinant of phenotypic expression of genetic change.
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	80149-5
ISSN	1879-3479 ; 0020-7292
ISSN (online)	1879-3479
ISSN	0020-7292
DOI	10.1002/ijgo.15486
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Zs.A 355: 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)
Zs.MO 183: Show issues

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