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Article ; Online: Iron chelation therapy to prevent poststroke cognitive impairments: role of diabetes and sex.

Sakamuri, Siva S V P / Sure, Venkata N / Katakam, Prasad V G

American journal of physiology. Heart and circulatory physiology

2023 Volume 324, Issue 2, Page(s) H210–H211

MeSH term(s)	Rats ; Female ; Animals ; Chelation Therapy ; Deferoxamine ; Diabetes Mellitus, Experimental ; Ferroptosis ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/prevention & control ; Iron ; Hemorrhage ; Stroke/prevention & control
Chemical Substances	Deferoxamine (J06Y7MXW4D) ; Iron (E1UOL152H7)
Language	English
Publishing date	2023-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00004.2023
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Article: Single cell regulatory architecture of human pancreatic islets suggests sex differences in β cell function and the pathogenesis of type 2 diabetes.

Qadir, Mirza Muhammad Fahd / Elgamal, Ruth M / Song, Keijing / Kudtarkar, Parul / Sakamuri, Siva S V P / Katakam, Prasad V / El-Dahr, Samir / Kolls, Jay / Gaulton, Kyle J / Mauvais-Jarvis, Franck

bioRxiv : the preprint server for biology

2024

Abstract: Biological sex affects the pathogenesis of type 2 and type 1 diabetes (T2D, T1D) including the development of β cell failure observed more often in males. The mechanisms that drive sex differences in β cell failure is unknown. Studying sex differences in ...

Abstract	Biological sex affects the pathogenesis of type 2 and type 1 diabetes (T2D, T1D) including the development of β cell failure observed more often in males. The mechanisms that drive sex differences in β cell failure is unknown. Studying sex differences in islet regulation and function represent a unique avenue to understand the sex-specific heterogeneity in β cell failure in diabetes. Here, we examined sex and race differences in human pancreatic islets from up to 52 donors with and without T2D (including 37 donors from the Human Pancreas Analysis Program [HPAP] dataset) using an orthogonal series of experiments including single cell RNA-seq (scRNA-seq), single nucleus assay for transposase-accessible chromatin sequencing (snATAC-seq), dynamic hormone secretion, and bioenergetics. In cultured islets from nondiabetic (ND) donors, in the absence of the
Language	English
Publishing date	2024-04-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.11.589096
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Article ; Online: Diets with low n-6:n-3 PUFA ratio protects rats from fructose-induced dyslipidemia and associated hepatic changes: Comparison between 18:3 n-3 and long-chain n-3 PUFA.

Sakamuri, Anil / Sakamuri, Siva S V P / Kona, Suryam Reddy / Jeyapal, Sugeedha / Ibrahim, Ahamed

Prostaglandins, leukotrienes, and essential fatty acids

2020 Volume 155, Page(s) 102082

Abstract: In the present study, we investigated the impact of substituting alpha-linolenic acid (ALA) or long-chain n-3 PUFA (eicosapentaenoic acid and docosahexaenoic acid) for linoleic acid and hence decreasing n-6:n-3 PUFA ratio on high-fructose diet-induced ... ...

Abstract	In the present study, we investigated the impact of substituting alpha-linolenic acid (ALA) or long-chain n-3 PUFA (eicosapentaenoic acid and docosahexaenoic acid) for linoleic acid and hence decreasing n-6:n-3 PUFA ratio on high-fructose diet-induced hypertriglyceridemia and associated hepatic changes. Weanling male Wistar rats were divided into four groups and fed with starch-diet (n-6:n-3 PUFA ratio 215:1) and high-fructose diets with different n-6:n-3 PUFA ratio (215:1, 2:1 with ALA and 5:1 with long-chain n-3 PUFA) for twenty-four weeks. Substitution of linoleic acid with ALA (n-6:n-3 PUFA ratio of 2) or long-chain n-3 PUFA (n-6:n-3 PUFA ratio of 5) protected the rats from fructose-induced dyslipidemia, hepatic oxidative stress and corrected lipogenic and proinflammatory gene expression. Both ALA and long-chain n-3 PUFA supplementation also reversed the fructose-induced upregulation of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) gene, which is involved in the generation of active glucocorticoids in tissues. Although both ALA and LC n-3 PUFA prevented fructose-induced dyslipidemia to a similar extent, compared to ALA, LC n-3 PUFA is more effective in preventing hepatic oxidative stress and inflammation.
MeSH term(s)	11-beta-Hydroxysteroid Dehydrogenase Type 1/genetics ; Animals ; Diet/methods ; Dyslipidemias/chemically induced ; Dyslipidemias/diet therapy ; Fructose/adverse effects ; Gene Expression Regulation/drug effects ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/prevention & control ; Linoleic Acid/administration & dosage ; Liver/metabolism ; Male ; Oxidative Stress/drug effects ; Rats ; Rats, Wistar ; alpha-Linolenic Acid/administration & dosage
Chemical Substances	alpha-Linolenic Acid (0RBV727H71) ; Fructose (30237-26-4) ; Linoleic Acid (9KJL21T0QJ) ; 11-beta-Hydroxysteroid Dehydrogenase Type 1 (EC 1.1.1.146)
Language	English
Publishing date	2020-02-22
Publishing country	Scotland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	286714-x
ISSN	1532-2823 ; 0952-3278
ISSN (online)	1532-2823
ISSN	0952-3278
DOI	10.1016/j.plefa.2020.102082
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Article ; Online: Amyloid [Formula: see text] (1-42) peptide impairs mitochondrial respiration in primary human brain microvascular endothelial cells: impact of dysglycemia and pre-senescence.

Sakamuri, Siva S V P / Sure, Venkata N / Wang, Xiaoying / Bix, Gregory / Fonseca, Vivian A / Mostany, Ricardo / Katakam, Prasad V G

GeroScience

2022 Volume 44, Issue 6, Page(s) 2721–2739

Abstract: Diabetes increases the risk of Alzheimer's disease (AD). We investigated the impact of glucose ...

Abstract	Diabetes increases the risk of Alzheimer's disease (AD). We investigated the impact of glucose concentrations on the β-amyloid (Aβ)-induced alteration of mitochondrial/cellular energetics in primary human brain microvascular endothelial cells (HBMECs). HBMECs were grown and passaged in media containing 15 mmol/l glucose (normal) based on which the glucose levels in the media were designated as high (25 mmol/L) or low (5 mmol/L). HBMECs were treated with Aβ (1-42) (5 µmol/l) or a scrambled peptide for 24 h and mitochondrial respiratory parameters were measured using Seahorse Mito Stress Test. Aβ (1-42) decreased the mitochondrial ATP production at normal glucose levels and decreased spare respiratory capacity at high glucose levels. Aβ (1-42) diminished all mitochondrial respiratory parameters markedly at low glucose levels that were not completely recovered by restoring normal glucose levels in the media. The addition of mannitol (10 mmol/l) to low and normal glucose-containing media altered the Aβ (1-42)-induced bioenergetic defects. Even at normal glucose levels, pre-senescent HMBECs (passage 15) displayed greater Aβ (1-42)-induced mitochondrial respiratory impairments than young cells (passages 7-9). Thus, hypoglycemia, osmolarity changes, and senescence are stronger instigators of Aβ (1-42)-induced mitochondrial respiration and energetics in HBMECs and contributors to diabetes-related increased AD risk than hyperglycemia.
MeSH term(s)	Humans ; Endothelial Cells ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Respiration ; Glucose/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-08-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-022-00644-x
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Article ; Online: Conditioned place avoidance is associated with a distinct hippocampal phenotype, partly preserved pattern separation, and reduced reactive oxygen species production after stress.

Kelley, D Parker / Albrechet-Souza, Lucas / Cruise, Shealan / Maiya, Rajani / Destouni, Aspasia / Sakamuri, Siva S V P / Duplooy, Alexander / Hibicke, Meghan / Nichols, Charles / Katakam, Prasad V G / Gilpin, Nicholas W / Francis, Joseph

Genes, brain, and behavior

2023 Volume 22, Issue 2, Page(s) e12840

Abstract: Stress is associated with contextual memory deficits, which may mediate avoidance of trauma-associated contexts in posttraumatic stress disorder. These deficits may emerge from impaired pattern separation, the independent representation of similar ... ...

Abstract	Stress is associated with contextual memory deficits, which may mediate avoidance of trauma-associated contexts in posttraumatic stress disorder. These deficits may emerge from impaired pattern separation, the independent representation of similar experiences by the dentate gyrus-Cornu Ammonis 3 (DG-CA3) circuit of the dorsal hippocampus, which allows for appropriate behavioral responses to specific environmental stimuli. Neurogenesis in the DG is controlled by mitochondrial reactive oxygen species (ROS) production, and may contribute to pattern separation. In Experiment 1, we performed RNA sequencing of the dorsal hippocampus 16 days after stress in rats that either develop conditioned place avoidance to a predator urine-associated context (Avoiders), or do not (Non-Avoiders). Weighted genome correlational network analysis showed that increased expression of oxidative phosphorylation-associated gene transcripts and decreased expression of gene transcripts for axon guidance and insulin signaling were associated with avoidance behavior. Based on these data, in Experiment 2, we hypothesized that Avoiders would exhibit elevated hippocampal (HPC) ROS production and degraded object pattern separation (OPS) compared with Nonavoiders. Stress impaired pattern separation performance in Non-Avoider and Avoider rats compared with nonstressed Controls, but surprisingly, Avoiders exhibited partly preserved pattern separation performance and significantly lower ROS production compared with Non-Avoiders. Lower ROS production was associated with better OPS performance in Stressed rats, but ROS production was not associated with OPS performance in Controls. These results suggest a strong negative association between HPC ROS production and pattern separation after stress, and that stress effects on these outcome variables may be associated with avoidance of a stress-paired context.
MeSH term(s)	Rats ; Animals ; Reactive Oxygen Species/pharmacology ; Hippocampus/metabolism ; CA3 Region, Hippocampal/metabolism ; Avoidance Learning/physiology ; Stress Disorders, Post-Traumatic ; Dentate Gyrus/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2023-02-17
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2075819-4
ISSN	1601-183X ; 1601-1848
ISSN (online)	1601-183X
ISSN	1601-1848
DOI	10.1111/gbb.12840
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Zs.A 5642: Show issues

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Article ; Online: Intermittent cytomegalovirus infection alters neurobiological metabolism and induces cognitive deficits in mice.

Harrison, Mark A A / Morris, Sara L / Rudman, Grace A / Rittenhouse, Daniel J / Monk, Chandler H / Sakamuri, Siva S V P / Mehedi Hasan, Md / Shamima Khatun, Mst / Wang, Hanyun / Garfinkel, Lucas P / Norton, Elizabeth B / Kim, Sangku / Kolls, Jay K / Michal Jazwinski, S / Mostany, Ricardo / Katakam, Prasad V G / Engler-Chiurazzi, Elizabeth B / Zwezdaryk, Kevin J

Brain, behavior, and immunity

2024 Volume 117, Page(s) 36–50

Abstract: Risk factors contributing to dementia are multifactorial. Accumulating evidence suggests a role for pathogens as risk factors, but data is largely correlative with few causal relationships. Here, we demonstrate that intermittent murine cytomegalovirus ( ... ...

Abstract	Risk factors contributing to dementia are multifactorial. Accumulating evidence suggests a role for pathogens as risk factors, but data is largely correlative with few causal relationships. Here, we demonstrate that intermittent murine cytomegalovirus (MCMV) infection of mice, alters blood brain barrier (BBB) permeability and metabolic pathways. Increased basal mitochondrial function is observed in brain microvessels cells (BMV) exposed to intermittent MCMV infection and is accompanied by elevated levels of superoxide. Further, mice score lower in cognitive assays compared to age-matched controls who were never administered MCMV. Our data show that repeated systemic infection with MCMV, increases markers of neuroinflammation, alters mitochondrial function, increases markers of oxidative stress and impacts cognition. Together, this suggests that viral burden may be a risk factor for dementia. These observations provide possible mechanistic insights through which pathogens may contribute to the progression or exacerbation of dementia.
MeSH term(s)	Animals ; Mice ; Cognitive Dysfunction ; Cognition Disorders ; Cytomegalovirus Infections/complications ; Cognition ; Dementia
Language	English
Publishing date	2024-01-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2023.12.033
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Architecture of androgen receptor pathways amplifying glucagon-like peptide-1 insulinotropic action in male pancreatic β cells

Weiwei Xu / M.M. Fahd Qadir / Daniela Nasteska / Paula Mota de Sa / Caroline M. Gorvin / Manuel Blandino-Rosano / Charles R. Evans / Thuong Ho / Evgeniy Potapenko / Rajakrishnan Veluthakal / Fiona B. Ashford / Stavroula Bitsi / Jia Fan / Manika Bhondeley / Kejing Song / Venkata N. Sure / Siva S.V.P. Sakamuri / Lina Schiffer / Wandy Beatty /

Rachael Wyatt / Daniel E. Frigo / Xiaowen Liu / Prasad V. Katakam / Wiebke Arlt / Jochen Buck / Lonny R. Levin / Tony Hu / Jay Kolls / Charles F. Burant / Alejandra Tomas / Matthew J. Merrins / Debbie C. Thurmond / Ernesto Bernal-Mizrachi / David J. Hodson / Franck Mauvais-Jarvis

Cell Reports, Vol 42, Iss 5, Pp 112529- (2023)

2023

Abstract: Summary: Male mice lacking the androgen receptor (AR) in pancreatic β cells exhibit blunted glucose-stimulated insulin secretion (GSIS), leading to hyperglycemia. Testosterone activates an extranuclear AR in β cells to amplify glucagon-like peptide-1 ( ... ...

Abstract	Summary: Male mice lacking the androgen receptor (AR) in pancreatic β cells exhibit blunted glucose-stimulated insulin secretion (GSIS), leading to hyperglycemia. Testosterone activates an extranuclear AR in β cells to amplify glucagon-like peptide-1 (GLP-1) insulinotropic action. Here, we examined the architecture of AR targets that regulate GLP-1 insulinotropic action in male β cells. Testosterone cooperates with GLP-1 to enhance cAMP production at the plasma membrane and endosomes via: (1) increased mitochondrial production of CO2, activating the HCO3−-sensitive soluble adenylate cyclase; and (2) increased Gαs recruitment to GLP-1 receptor and AR complexes, activating transmembrane adenylate cyclase. Additionally, testosterone enhances GSIS in human islets via a focal adhesion kinase/SRC/phosphatidylinositol 3-kinase/mammalian target of rapamycin complex 2 actin remodeling cascade. We describe the testosterone-stimulated AR interactome, transcriptome, proteome, and metabolome that contribute to these effects. This study identifies AR genomic and non-genomic actions that enhance GLP-1-stimulated insulin exocytosis in male β cells.
Keywords	CP: Metabolism ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article: TRAF3IP2 mediates aldosterone/salt-induced cardiac hypertrophy and fibrosis

Sakamuri, Siva S.V.P / Anthony J. Valente / Chandrasekar Bysani / Jalahalli M. Siddesha / Jason D. Gardner / Patrice Delafontaine / Ulrich Siebenlist

Molecular and Cellular Endocrinology. 2016 July 05, v. 429

2016

Abstract: Aberrant activation of the renin-angiotensin-aldosterone system (RAAS) contributes to adverse cardiac remodeling and eventual failure. Here we investigated whether TRAF3 Interacting Protein 2 (TRAF3IP2), a redox-sensitive cytoplasmic adaptor molecule and ...

Abstract	Aberrant activation of the renin-angiotensin-aldosterone system (RAAS) contributes to adverse cardiac remodeling and eventual failure. Here we investigated whether TRAF3 Interacting Protein 2 (TRAF3IP2), a redox-sensitive cytoplasmic adaptor molecule and an upstream regulator of nuclear factor-ÎºB (NF-ÎºB) and activator protein-1 (AP-1), mediates aldosterone-induced cardiac hypertrophy and fibrosis. Wild type (WT) and TRAF3IP2-null mice were infused with aldosterone (0.2Â mg/kg/day) for 4 weeks along with 1%NaCl in drinking water. Aldosterone/salt, but not salt alone, upregulated TRAF3IP2 expression in WT mouse hearts. Further, aldosterone elevated blood pressure to a similar extent in both WT and TRAF3IP2-null groups. However, TRAF3IP2 gene deletion attenuated aldosterone/salt-induced (i) p65 and c-Jun activation, (ii) extracellular matrix (collagen IÎ±1 and collagen IIIÎ±1), matrix metalloproteinase (MMP2), lysyl oxidase (LOX), inflammatory cytokine (IL-6 and IL-18), chemokine (CXCL1 and CXCL2), and adhesion molecule (ICAM1) mRNA expression in hearts, (iii) IL-6, IL-18, and MMP2 protein levels, (iv) systemic IL-6 and IL-18 levels, and (iv) cardiac hypertrophy and fibrosis. These results indicate that TRAF3IP2 is a critical signaling intermediate in aldosterone/salt-induced myocardial hypertrophy and fibrosis, and thus a potential therapeutic target in hypertensive heart disease.
Keywords	adhesion ; aldosterone ; blood pressure ; chemokine CXCL1 ; chemokine CXCL2 ; collagen ; drinking water ; extracellular matrix ; fibrosis ; gene deletion ; gene expression ; heart ; heart diseases ; hypertrophy ; interleukin-18 ; interleukin-6 ; messenger RNA ; metalloproteinases ; mice ; transcription factor NF-kappa B
Language	English
Dates of publication	2016-0705
Size	p. 84-92.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2016.03.038
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: High-plasma soluble prorenin receptor is associated with vascular damage in male, but not female, mice fed a high-fat diet.

Visniauskas, Bruna / Reverte, Virginia / Abshire, Caleb M / Ogola, Benard O / Rosales, Carla B / Galeas-Pena, Michelle / Sure, Venkata N / Sakamuri, Siva S V P / Harris, Nicholas R / Kilanowski-Doroh, Isabella / Mcnally, Alexandra B / Horton, Alec C / Zimmerman, Margaret / Katakam, Prasad V G / Lindsey, Sarah H / Prieto, Minolfa C

American journal of physiology. Heart and circulatory physiology

2023 Volume 324, Issue 6, Page(s) H762–H775

Abstract: Plasma soluble prorenin receptor (sPRR) displays sexual dimorphism and is higher in women with type 2 diabetes mellitus (T2DM). However, the contribution of plasma sPRR to the development of vascular complications in T2DM remains unclear. We investigated ...

Abstract	Plasma soluble prorenin receptor (sPRR) displays sexual dimorphism and is higher in women with type 2 diabetes mellitus (T2DM). However, the contribution of plasma sPRR to the development of vascular complications in T2DM remains unclear. We investigated if plasma sPRR contributes to sex differences in the activation of the systemic renin-angiotensin-aldosterone system (RAAS) and vascular damage in a model of high-fat diet (HFD)-induced T2DM. Male and female C57BL/6J mice were fed either a normal fat diet (NFD) or an HFD for 28 wk to assess changes in blood pressure, cardiometabolic phenotype, plasma prorenin/renin, sPRR, and ANG II. After completing dietary protocols, tissues were collected from males to assess vascular reactivity and aortic reactive oxygen species (ROS). A cohort of male mice was used to determine the direct contribution of increased systemic sPRR by infusion. To investigate the role of ovarian hormones, ovariectomy (OVX) was performed at 32 wk in females fed either an NFD or HFD. Significant sex differences were found after 28 wk of HFD, where only males developed T2DM and increased plasma prorenin/renin, sPRR, and ANG II. T2DM in males was accompanied by nondipping hypertension, carotid artery stiffening, and aortic ROS. sPRR infusion in males induced vascular thickening instead of material stiffening caused by HFD-induced T2DM. While intact females were less prone to T2DM, OVX increased plasma prorenin/renin, sPRR, and systolic blood pressure. These data suggest that sPRR is a novel indicator of systemic RAAS activation and reflects the onset of vascular complications during T2DM regulated by sex.
MeSH term(s)	Female ; Male ; Mice ; Animals ; Renin ; Prorenin Receptor ; Diabetes Mellitus, Type 2 ; Diet, High-Fat/adverse effects ; Reactive Oxygen Species ; Mice, Inbred C57BL ; Renin-Angiotensin System/genetics ; Hypertension ; Receptors, Cell Surface/genetics ; Blood Pressure ; Vacuolar Proton-Translocating ATPases
Chemical Substances	Renin (EC 3.4.23.15) ; Prorenin Receptor ; Reactive Oxygen Species ; N-formyl-13-dihydrocarminomycin (76634-96-3) ; Receptors, Cell Surface ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
Language	English
Publishing date	2023-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00638.2022
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Article ; Online: Glycolytic and Oxidative Phosphorylation Defects Precede the Development of Senescence in Primary Human Brain Microvascular Endothelial Cells.

Sakamuri, Siva S V P / Sure, Venkata N / Kolli, Lahari / Liu, Ning / Evans, Wesley R / Sperling, Jared A / Busija, David W / Wang, Xiaoying / Lindsey, Sarah H / Murfee, Walter L / Mostany, Ricardo / Katakam, Prasad V G

GeroScience

2022 Volume 44, Issue 4, Page(s) 1975–1994

Abstract: Alterations of mitochondrial and glycolytic energy pathways related to aging could contribute to cerebrovascular dysfunction. We studied the impact of aging on energetics of primary human brain microvascular endothelial cells (HBMECs) by comparing the ... ...

Abstract	Alterations of mitochondrial and glycolytic energy pathways related to aging could contribute to cerebrovascular dysfunction. We studied the impact of aging on energetics of primary human brain microvascular endothelial cells (HBMECs) by comparing the young (passages 7-9), pre-senescent (passages 13-15), and senescent (passages 20-21) cells. Pre-senescent HBMECs displayed decreased telomere length and undetectable telomerase activity although markers of senescence were unaffected. Bioenergetics in HBMECs were determined by measuring the oxygen consumption (OCR) and extracellular acidification (ECAR) rates. Cellular ATP production in young HBMECs was predominantly dependent on glycolysis with glutamine as the preferred fuel for mitochondrial oxidative phosphorylation (OXPHOS). In contrast, pre-senescent HBMECs displayed equal contribution to ATP production rate from glycolysis and OXPHOS with equal utilization of glutamine, glucose, and fatty acids as mitofuels. Compared to young, pre-senescent HBMECs showed a lower overall ATP production rate that was characterized by diminished contribution from glycolysis. Impairments of glycolysis displayed by pre-senescent cells included reduced basal glycolysis, compensatory glycolysis, and non-glycolytic acidification. Furthermore, impairments of mitochondrial respiration in pre-senescent cells involved the reduction of maximal respiration and spare respiratory capacity but intact basal and ATP production-related OCR. Proton leak and non-mitochondrial respiration, however, were unchanged in the pre-senescent HBMECs. HBMECS at passages 20-21 displayed expression of senescence markers and continued similar defects in glycolysis and worsened OXPHOS. Thus, for the first time, we characterized the bioenergetics of pre-senescent HBMECs comprehensively to identify the alterations of the energy pathways that could contribute to aging.
MeSH term(s)	Humans ; Oxidative Phosphorylation ; Endothelial Cells ; Glutamine/metabolism ; Glycolysis ; Brain/metabolism ; Adenosine Triphosphate/metabolism
Chemical Substances	Glutamine (0RH81L854J) ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2022-04-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-022-00550-2
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Inter-library loan at ZB MED

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito