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Article ; Online: Interplay of mitochondria-associated membrane proteins and autophagy: Implications in neurodegeneration.

Kulkarni, Prakash G / Mohire, Vaibhavi M / Waghmare, Pranjal P / Banerjee, Tanushree

2024 Volume 76, Page(s) 101874

Abstract: Since the discovery of membrane contact sites between ER and mitochondria called mitochondria-associated membranes (MAMs), several pieces of evidence identified their role in the regulation of different cellular processes such as ... ...

Abstract	Since the discovery of membrane contact sites between ER and mitochondria called mitochondria-associated membranes (MAMs), several pieces of evidence identified their role in the regulation of different cellular processes such as Ca
Language	English
Publishing date	2024-03-20
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2024.101874
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Article ; Online: DNA Methylation-Mediated Mfn2 Gene Regulation in the Brain: A Role in Brain Trauma-Induced Mitochondrial Dysfunction and Memory Deficits.

Kulkarni, Prakash G / Balasubramanian, Nagalakshmi / Manjrekar, Ritika / Banerjee, Tanushree / Sakharkar, Amul

Cellular and molecular neurobiology

2023 Volume 43, Issue 7, Page(s) 3479–3495

Abstract: Repeated mild traumatic brain injuries (rMTBI) affect mitochondrial homeostasis in the brain. However, mechanisms of long-lasting neurobehavioral effects of rMTBI are largely unknown. Mitofusin 2 (Mfn2) is a critical component of tethering complexes in ... ...

Abstract	Repeated mild traumatic brain injuries (rMTBI) affect mitochondrial homeostasis in the brain. However, mechanisms of long-lasting neurobehavioral effects of rMTBI are largely unknown. Mitofusin 2 (Mfn2) is a critical component of tethering complexes in mitochondria-associated membranes (MAMs) and thereby plays a pivotal role in mitochondrial functions. Herein, we investigated the implications of DNA methylation in the Mfn2 gene regulation, and its consequences on mitochondrial dysfunction in the hippocampus after rMTBI. rMTBI dramatically reduced the mitochondrial mass, which was concomitant with decrease in Mfn2 mRNA and protein levels. DNA hypermethylation at the Mfn2 gene promoter was observed post 30 days of rMTBI. The treatment of 5-Azacytidine, a pan DNA methyltransferase inhibitor, normalized DNA methylation levels at Mfn2 promoter, which further resulted into restoration of Mfn2 function. The normalization of Mfn2 function was well correlated with recovery in memory deficits in rMTBI-exposed rats. Since, glutamate excitotoxicity serves as a primary insult after TBI, we employed in vitro model of glutamate excitotoxicity in human neuronal cell line SH-SY5Y to investigate the causal epigenetic mechanisms of Mfn2 gene regulation. The glutamate excitotoxicity reduced Mfn2 levels via DNA hypermethylation at Mfn2 promoter. Loss of Mfn2 caused significant surge in cellular and mitochondrial ROS levels with lowered mitochondrial membrane potential in cultured SH-SY5Y cells. Like rMTBI, these consequences of glutamate excitotoxicity were also prevented by 5-AzaC pre-treatment. Therefore, DNA methylation serves as a vital epigenetic mechanism involved in Mfn2 expression in the brain; and this Mfn2 gene regulation may play a pivotal role in rMTBI-induced persistent cognitive deficits. Closed head weight drop injury method was employed to induce repeated mild traumatic brain (rMTBI) in jury in adult, male Wistar rats. rMTBI causes hyper DNA methylation at the Mfn2 promoter and lowers the Mfn2 expression triggering mitochondrial dysfunction. However, the treatment of 5-azacytidine normalizes DNA methylation at the Mfn2 promoter and restores mitochondrial function.
MeSH term(s)	Animals ; Male ; Rats ; Azacitidine/pharmacology ; Brain/metabolism ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/genetics ; Brain Injuries, Traumatic/metabolism ; DNA/metabolism ; DNA Methylation ; Glutamates/metabolism ; Memory Disorders/etiology ; Mitochondria/metabolism ; Neuroblastoma ; Rats, Wistar
Chemical Substances	Azacitidine (M801H13NRU) ; DNA (9007-49-2) ; Glutamates ; Mfn2 protein, rat (EC 3.6.1.-)
Language	English
Publishing date	2023-05-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-023-01358-0
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Article ; Online: Understanding the role of nACE2 in neurogenic hypertension among COVID-19 patients.

Kulkarni, Prakash G / Sakharkar, Amul / Banerjee, Tanushree

Hypertension research : official journal of the Japanese Society of Hypertension

2021 Volume 45, Issue 2, Page(s) 254–269

Abstract: Currently, the third and fourth waves of the coronavirus disease -19 (COVID-19) pandemic are creating havoc in many parts of the world. Although vaccination programs have been launched in most countries, emerging new strains of the virus along with ... ...

Abstract	Currently, the third and fourth waves of the coronavirus disease -19 (COVID-19) pandemic are creating havoc in many parts of the world. Although vaccination programs have been launched in most countries, emerging new strains of the virus along with geographical variations are leading to varying success rates of the available vaccines. The presence of comorbidities such as diabetes, cardiovascular diseases and hypertension is responsible for increasing the severity of COVID-19 and, thus, the COVID-19 mortality rate. Angiotensin-converting enzyme 2 (ACE2), which is utilized by SARS-CoV-2 for entry into host cells, is widely expressed in the lungs, kidneys, testes, gut, adipose tissue, and brain. Infection within host cells mediates RAS overactivation, which leads to a decrease in the ACE2/ACE ratio, AT2R/AT1R ratio, and MasR/AT1R ratio. Such imbalances lead to the development of heightened inflammatory responses, such as cytokine storms, leading to post-COVID-19 complications and mortality. As the association of SARS-CoV-2 infection and hypertension remains unclear, this report provides an overview of the effects of SARS-CoV-2 infection on patients with hypertension. We discuss here the interaction of ACE2 with SARS-CoV-2, focusing on neuronal ACE2 (nACE2), and further shed light on the possible involvement of nACE2 in hypertension. SARS-CoV-2 enters the brain through neuronal ACE2 and spreads in various regions of the brain. The effect of viral binding to neuronal ACE2 in areas of the brain that regulate salt/water balance and blood pressure is also discussed in light of the neural regulation of hypertension in COVID-19.
MeSH term(s)	Angiotensin-Converting Enzyme 2 ; COVID-19 ; Humans ; Hypertension ; Peptidyl-Dipeptidase A/metabolism ; Renin-Angiotensin System ; SARS-CoV-2
Chemical Substances	Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2021-11-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1175297-x
ISSN	1348-4214 ; 0916-9636
ISSN (online)	1348-4214
ISSN	0916-9636
DOI	10.1038/s41440-021-00800-4
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Article: Evaluation of Uric Acid to Albumin Ratio as a Marker of Coronary Artery Disease Severity in Acute Coronary Syndrome: A Cross-Sectional Study.

Sultana, Sana / K, Mohammed Suhail / Prakash, Varsha Rakshitha / Karthikeyan, Aditya / Aslam S, Shaikh Mohammed / C, Suhas G / Kulkarni, Ashwin

Cureus

2023 Volume 15, Issue 11, Page(s) e49454

Abstract: Background: Coronary artery disease (CAD) is a widespread cause of morbidity and mortality. Serum uric acid, a mediator of endothelial dysfunction and inflammation in vascular disease, can increase the risk of atherosclerosis, contributing to CAD. As ... ...

Abstract	Background: Coronary artery disease (CAD) is a widespread cause of morbidity and mortality. Serum uric acid, a mediator of endothelial dysfunction and inflammation in vascular disease, can increase the risk of atherosclerosis, contributing to CAD. As serum albumin inhibits platelet activation and aggregation, low levels of it can contribute to platelet-induced coronary artery stenosis. Limited studies have been conducted worldwide in evaluating the role of uric acid to albumin ratio (UAR) in predicting severity or poor outcomes in acute coronary syndrome (ACS) patients. This study was undertaken to assess the role of UAR as a predictor of CAD severity, which can facilitate the identification of high-risk patients. Methodology: A hospital-based analytical cross-sectional study was conducted in an urban tertiary healthcare center for a period of two months between June and August of 2022. A total of 100 ACS patients were included in the study. The study population included patients above the age of 18 years diagnosed with ACS who underwent a coronary angiography. Coronary angiograms were used to diagnose the presence of CAD, and its severity was assessed using Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) scores (SS). The correlation of UAR with CAD severity using SS was studied and compared between three varieties of ACS: ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina (UA). Statistics: Chi-squared tests were used to determine statistical significance for qualitative data. Independent t-tests were used to identify the mean difference between two quantitative variables. Receiver operating characteristic (ROC) curves were constructed for UAR and high SS. A comparison between UAR and neutrophil to lymphocyte ratio (NLR) as a predictor of disease severity was done. ROC and optimal cutoff points were chosen to calculate sensitivity, specificity, and positive and negative predictive values. Microsoft Excel (Microsoft, Redmond, WA, USA) and SPSS V22.0 (IBM Corp., Armonk, NY, USA) were used to analyze the data. Results: A total of 100 ACS patients were included in the study and divided into two groups on the basis of SS, with 74% showing low severity and 26% showing intermediate-high severity. There was a statistically significant difference found between older age and SS (p=0.017). Our study showed 74% (n=74) of the patients were male and 26% (n=26) were female. It also revealed that 75.7% (n=56) of the male patients were in the low-severity group, and 24.3% (n=18) of males were in the intermediate-high severity group. 69.2% (n=18) of the female patients were in the low-severity group, and 30.8% (n=8) were in the intermediate-high severity group. Of the 100 patients, 55% were diagnosed with STEMI, of which 69.1% were in the low-severity group, and 30.9% were in the intermediate-high severity group. Among all the patients 33% of the patients were diagnosed as NSTEMI, of which 72.7% were in the low-severity group, and 27.3% were in the intermediate-high severity group. Twelve percent of the patients were diagnosed with UA, and 100% of these patients were in the low-severity group. The mean UAR was 1.40 ± 0.38 in the low-severity group and 1.29 ± 0.46 in the intermediate-high severity group (p=0.22). Conclusion: Our study yielded no statistically significant difference in UAR among varying severities of CAD.
Language	English
Publishing date	2023-11-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2747273-5
ISSN	2168-8184
ISSN	2168-8184
DOI	10.7759/cureus.49454
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Article: A Case of Hearing Impairment with Renal Dysfunction.

Prakash, G K / Kulkarni, Sagar C / Rashmi, S R / Mahesha, V / Vishwanath, S / Ballal, H S

Indian journal of nephrology

2021 Volume 31, Issue 1, Page(s) 64–66

Abstract: Hearing impairment in a patient with renal failure is an important clue towards etiologic diagnosis of kidney disease. Variety of hereditary diseases, developmental defects, and toxins involve these two organs. However, additional retinopathy is seen in ... ...

Abstract	Hearing impairment in a patient with renal failure is an important clue towards etiologic diagnosis of kidney disease. Variety of hereditary diseases, developmental defects, and toxins involve these two organs. However, additional retinopathy is seen in quite a few diseases which include Alport's syndrome and Muckle-Wells syndrome (MWS). We are reporting a case of middle-aged woman with childhood-onset of hearing impairment who presented with renal failure and was diagnosed to have renal amyloidosis on kidney biopsy but without any light chain restriction. During evaluation for live donor kidney transplant, her brother was also found to have hearing impairment and retinopathy however with normal renal function and urinalysis. Genetic testing of both of them was done for panel of mutations related to hereditary amyloidosis which revealed NLRP3 mutation in both. This mutation is characteristic of MWS which can lead to secondary amyloidosis and renal failure.
Language	English
Publishing date	2021-01-27
Publishing country	India
Document type	Case Reports
ZDB-ID	2134388-3
ISSN	1998-3662 ; 0971-4065
ISSN (online)	1998-3662
ISSN	0971-4065
DOI	10.4103/ijn.IJN_190_19
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Article ; Online: Corrigendum to Proteomic analysis detects deregulated reverse cholesterol transport in human subjects with ST-segment elevation myocardial infarction.

Das, Apabrita Ayan / Choudhury, Kamalika Roy / Jagadeeshaprasad, M G / Kulkarni, Mahesh J / Mondal, Prakash Chandra / Bandyopadhyay, Arun

Journal of proteomics

2022 Volume 260, Page(s) 104546

Language	English
Publishing date	2022-03-24
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2022.104546
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Article ; Online: Mitofusin-2: Functional switch between mitochondrial function and neurodegeneration.

Kulkarni, Prakash G / Mohire, Vaibhavi M / Bhaisa, Pooja K / Joshi, Mrudula M / Puranik, Chitranshi M / Waghmare, Pranjal P / Banerjee, Tanushree

Mitochondrion

2023 Volume 69, Page(s) 116–129

Abstract: Mitochondria are highly dynamic organelles known to play role in the regulation of several cellular biological processes. However, their dynamics such as number, shape, and biological functions are regulated by mitochondrial fusion and fission process. ... ...

Abstract	Mitochondria are highly dynamic organelles known to play role in the regulation of several cellular biological processes. However, their dynamics such as number, shape, and biological functions are regulated by mitochondrial fusion and fission process. The balance between the fusion and fission process is most important for the maintenance of mitochondrial structure as well as cellular functions. The alterations within mitochondrial dynamic processes were found to be associated with the progression of neurodegenerative diseases. In recent years, mitofusin-2 (Mfn2), a GTPase has emerged as a multifunctional protein which not only is found to regulate the mitochondrial fusion-fission process but also known to regulate several cellular functions such as mitochondrial metabolism, cellular biogenesis, signalling, and apoptosis via maintaining the ER-mitochondria contact sites. In this review, we summarize the current knowledge of the structural and functional properties of the Mfn2, its transcriptional regulation and their roles in several cellular functions with a focus on current advances in the pathogenesis of neurodegenerative diseases.
MeSH term(s)	Humans ; Apoptosis ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Mitochondria/metabolism ; Mitochondrial Dynamics/physiology ; Mitochondrial Proteins/metabolism ; Neurodegenerative Diseases/metabolism
Chemical Substances	GTP Phosphohydrolases (EC 3.6.1.-) ; Mitochondrial Proteins ; MFN2 protein, human (EC 3.6.1.-)
Language	English
Publishing date	2023-02-09
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2023.02.001
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Article ; Online: Intrinsically disordered proteins and conformational noise: The hypothesis a decade later.

Kulkarni, Prakash / Salgia, Ravi / Rangarajan, Govindan

iScience

2023 Volume 26, Issue 7, Page(s) 107109

Abstract: Phenotypic plasticity is the ability of individual genotypes to produce different phenotypes in response to environmental perturbations. We previously postulated how conformational noise emanating from conformational dynamics of intrinsically disordered ... ...

Abstract	Phenotypic plasticity is the ability of individual genotypes to produce different phenotypes in response to environmental perturbations. We previously postulated how conformational noise emanating from conformational dynamics of intrinsically disordered proteins (IDPs) which is distinct from transcriptional noise, can contribute to phenotypic switching by rewiring the cellular protein interaction network. Since most transcription factors are IDPs, we posited that conformational noise is an integral component of transcriptional noise implying that IDPs may amplify total noise in the system either stochastically or in response to environmental changes. Here, we review progress in elucidating the details of the hypothesis. We highlight empirical evidence supporting the hypothesis, discuss conceptual advances that underscore its fundamental importance and implications, and identify areas for future investigations.
Language	English
Publishing date	2023-06-15
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.107109
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Article: Lipoma Arborescens - Eyes See What Mind Knows!

Kulkarni, Himanshu Gurunath / Kulkarni, Gurunath S / Kulkarni, Prakash G

Journal of orthopaedic case reports

2017 Volume 7, Issue 5, Page(s) 59–62

Abstract: Introduction: Lipoma arborescens is a rare lesion, benign in nature and was first described in detail in 1957. <200 cases have been reported in the literature by now. It consists of subsynovial villous proliferation of mature fat cells. Since the ... ...

Abstract	Introduction: Lipoma arborescens is a rare lesion, benign in nature and was first described in detail in 1957. <200 cases have been reported in the literature by now. It consists of subsynovial villous proliferation of mature fat cells. Since the incidence of the condition is very rare, definite etiology has not established. Arthroscopic or open synovectomy has been the treatment of choice of the lesion. Case report: We present you a case of lipomatosis arborescens of the right knee in a 28-year-old male. The magnetic resonance imaging images showed high signal intensity villous or nodular foci on both T1- and T2-weighted images which were indicative of fat globules. They were predominantly found in huge number in suprapatellar pouch. The patient underwent arthroscopic synovectomy showing numerous broad- based polypoid or thin papillary villi composed of fatty tissue. Approximately 40 cc of lobulated globules were removed, and some were sent to histopathology which confirmed the presence of benign synovial tissue and fragments of adipose tissue present beneath the synovial surface. On 1-year follow-up, the patient was free of pain and devoid of any mechanical symptoms. Conclusion: Hence, we conclude that this is a rare entity that needs early intervention to prevent progressive joint degeneration and has excellent patient satisfaction with arthroscopic debridement with very low incidence of recurrence.
Language	English
Publishing date	2017-12-14
Publishing country	India
Document type	Case Reports
ZDB-ID	2658169-3
ISSN	2250-0685
ISSN	2250-0685
DOI	10.13107/jocr.2250-0685.896
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Article ; Online: Pharmacological blockade of HDAC6 attenuates cancer progression by inhibiting IL-1β and modulating immunosuppressive response in OSCC.

Mahale, Ashutosh / Routholla, Ganesh / Lavanya, S / Sharma, Pravesh / Ghosh, Balaram / Kulkarni, Onkar Prakash

International immunopharmacology

2024 Volume 132, Page(s) 111921

Abstract: Interleukin-1-beta (IL-1β) one of the biomarkers for oral squamous cell carcinoma (OSCC), is upregulated in tumor-microenvironment (TME) and associated with poor patient survival. Thus, a novel modulator of IL-1β would be of great therapeutic value for ... ...

Abstract	Interleukin-1-beta (IL-1β) one of the biomarkers for oral squamous cell carcinoma (OSCC), is upregulated in tumor-microenvironment (TME) and associated with poor patient survival. Thus, a novel modulator of IL-1β would be of great therapeutic value for OSCC treatment. Here we report regulation of IL-1β and TME by histone deacetylase-6 (HDAC6)-inhibitor in OSCC. We observed significant upregulation of HDAC6 in 4-nitroquniline (4-NQO)-induced OSCC in mice and 4-NQO & Lipopolysaccharide (LPS) stimulated OSCC and fibroblast cells. Tubastatin A (TSA)-attenuated the OSCC progression in mice as observed improvement in the histology over tongue and esophagus, with reduced tumor burden. TSA treatment to 4-NQO mice attenuated protein expression of HDAC6, pro-and-mature-IL-1β and pro-and-cleaved-caspase-1 and ameliorated acetylated-tubulin. In support of our experimental work, human TCGA analysis revealed HDAC6 and IL-1β were upregulated in the primary tumor, with different tumor stages and grades. We found TSA modulate TME, indicated by downregulation of CD11b
Language	English
Publishing date	2024-03-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2024.111921
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