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4. Looking backward to plan forward

Author

Lindsey, Merry L., primary, Kirk, Jonathan A., additional, LeBlanc, Amanda J., additional, Brunt, Keith R., additional, Carter, Jason R., additional, Hansell Keehan, Kara, additional, Ripplinger, Crystal M., additional, Kleinbongard, Petra, additional, and Kassiri, Zamaneh, additional

Published
2024
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5. The heart of physiological reports

Author

Lindsey, Merry L., primary, Brunt, Keith R., additional, Kleinbongard, Petra, additional, Carter, Jason R., additional, Ripplinger, Crystal M., additional, Kassiri, Zamaneh, additional, Hansell Keehan, Kara, additional, LeBlanc, Amanda J., additional, and Kirk, Jonathan A., additional

Published
2024
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8. We asked and you answered

Author

Lindsey, Merry L., primary, Kleinbongard, Petra, additional, Kassiri, Zamaneh, additional, Carter, Jason R., additional, Hansell Keehan, Kara, additional, Ripplinger, Crystal M., additional, LeBlanc, Amanda J., additional, Brunt, Keith R., additional, and Kirk, Jonathan A., additional

Published
2023
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9. Sex still matters in cardiovascular research

Author

Lindsey, Merry L., primary, Carter, Jason R., additional, Ripplinger, Crystal M., additional, Kassiri, Zamaneh, additional, Hansell Keehan, Kara, additional, Brunt, Keith R., additional, Kirk, Jonathan A., additional, Kleinbongard, Petra, additional, and LeBlanc, Amanda J., additional

Published
2023
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18. Estrogen replacement restores flow-induced vasodilation in coronary arterioles of aged and ovariectomized rats

Author

LeBlanc, Amanda J., Reyes, Rafael, Kang, Lori S., Dailey, Robert A., Stallone, John N., Moningka, Natasha C., and Muller-Delp, Judy M.

Subjects
Estrogen -- Physiological aspects, Estrogen -- Research, Nitric oxide -- Physiological aspects, Nitric oxide -- Research, Blood vessels -- Dilatation, Blood vessels -- Research, Biological sciences
Abstract

LeBianc A J, Reyes R, Kang LS, Dailey RA, Stallone JN, Moningka NC, Muller-Delp JM. Estrogen replacement restores fiow-induced vasodilation in coronary arterioles of aged and ovariectomized rats. Am J Physiol Regul Integr Comp Physiol 297: R1713-R1723, 2009. First published October 7, 2009; doi: 10.1152/ajpregu.00178.2009.--The risk for cardiovascular disease (CVD) increases with advancing age; however, the age at which CVD risk increases significantly is delayed by more than a decade in women compared with men. This cardioprotection, which women experience until menopause, is presumably due to the presence of ovarian hormones, in particular, estrogen. The purpose of this study was to determine how age and ovarian hormones affect flow-induced vasodilation in the coronary resistance vasculature. Coronary arterioles were isolated from young (6 mo), middle-aged (14 mo), and old (24 mo) intact, ovariectomized (OVX), and ovariectomized + estrogen replaced (OVE) female Fischer-344 rats to assess flow-induced vasodilation. Advancing age impaired flow-induced dilation of coronary arterioles (young: 50 [+ or -] 4 vs. old: 34 [+ or -] 6; % relaxation). Ovariectomy reduced flow-induced dilation in arterioles from young females, and estrogen replacement restored vasodilation to flow. In aged females, flow-induced vasodilation of arterioles was unaltered by OVX; however, estrogen replacement improved flow-induced dilation by ~160%. The contribution of nitric oxide (NO) to flow-induced dilation, assessed by nitric oxide synthase (NOS) inhibition with [N.sup.g]-nitro-L-arginine methyl ester (L-NAME), declined with age. L-NAME did not alter flow-induced vasodilation in arterioles from OVX rats, regardless of age. In contrast, L-NAME reduced flow-induced vasodilation of arterioles from estrogen-replaced rats at all ages. These findings indicate that the age-induced decline of flow-induced, NO-mediated dilation in coronary arterioles of female rats is related, in part, to a loss of ovarian estrogen, and estrogen supplementation can improve flow-induced dilation, even at an advanced age. endothelial nitric oxide synthase; Akt; nitric oxide; ovariectomy doi: 10.1152/ajpregu.00178.2009

Published
2009

19. We are the change we seek

Author

Lindsey, Merry L., primary, Kassiri, Zamaneh, additional, Hansell Keehan, Kara, additional, Brunt, Keith R., additional, Carter, Jason R., additional, Kirk, Jonathan A., additional, Kleinbongard, Petra, additional, LeBlanc, Amanda J., additional, and Ripplinger, Crystal M., additional

Published
2021
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20. Age impairs Flk-1 signaling and NO-mediated vasodilation in coronary arterioles

Author

LeBlanc, Amanda J., Shipley, Robert D., Kang, Lori S., and Muller-Delp, Judy M.

Subjects
Protein kinases -- Physiological aspects, Aging -- Physiological aspects, Nitric oxide -- Health aspects, Blood vessels -- Dilatation, Blood vessels -- Research, Biological sciences
Abstract

Impairment of flow-induced vasodilation in coronary resistance arterioles may contribute to the decline in coronary vasodilatory reserve that occurs with advancing age. This study investigated the effects of age on flow-induced signaling and activation of nitric oxide (NO)-mediated vasodilation in coronary resistance arterioles. Coronary arterioles were isolated from young (~6 mo) and old (~24 mo) male Fischer-344 rats to assess vasodilation to flow, vascular endothelial growth factor (VEGF), and ACh. Flow- and VEGF-induced vasodilation of coronary arterioles was impaired with age (P [less than or equal to] 0.05); however, ACh-induced vasodilation was preserved with age. [N.sup.G]-nitro-L-arginine methyl ester (L-NAME) (1 x [10.sup.-5] M) eliminated vasodilation to flow, VEGF, and ACh, indicating dependence of these responses on NO. SU-1498, an inhibitor of vascular endothelial growth factor receptor 2 (VEGFR, also known as Flk-1), abolished age-related differences in flow-induced vasodilation. Flow-stimulated phosphorylation of Flk-1 in coronary arterioles from young but not old rats and Flk-1 protein was reduced in coronary arterioles from old rats compared with those from young rats. Flow stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) in coronary arterioles from both young and old rats. VEGF induced phosphorylation of both protein kinase B (Akt) and eNOS in coronary arterioles. VEGF-induced phosphorylation of Akt, but not eNOS, was significantly reduced in arterioles from old rats compared with arterioles from young rats. Wortmannin, an inhibitor of phosphatidylinositol (PI) 3-kinase, eliminated age-related differences in both flow- and VEGF-induced vasodilation. These results indicate that impairment of Flk-1/PI3-kinase signaling contributes to the reduction of flow-induced vasodilation in coronary arterioles with advancing age. phosphatidylinositol 3-kinase; endothelial nitric oxide synthase; acetylcholine; vascular endothelial growth factor; phosphorylated endothelial nitric oxide synthase; phophorylated protein kinase B; vasodilation

Published
2008

30. We are the change we seek.

Author

Lindsey, Merry L., Kassiri, Zamaneh, Keehan, Kara Hansell, Brunt, Keith R., Carter, Jason R., Kirk, Jonathan A., Kleinbongard, Petra, LeBlanc, Amanda J., and Ripplinger, Crystal M.

Subjects
MYOCARDIAL reperfusion, SCIENTIFIC communication, CYTOLOGY
Abstract

FormembersoftheAmericanPhysiologicalSociety(APS), particularly those affiliated with the Cardiovascular Section (CV Section), AJP-Heart and Circ is a natural home for their publications. Am J Physiol Heart Circ Physiol 317: H891-H922, 2019 [Erratum in Am J Physiol Heart Circ Physiol 317: H1390, 2019]. doi:10.1152/ajpheart.00259.2019. AJP-Heart and Circ has a robust presence on Twitter, Facebook, and Instagram, and our Consulting Editors will amplify our social media messaging on their own professional social media profiles. Perhaps most importantly, the AJP-Heart and Circ editorial team envisions the new role of Consulting Editor to serve as ambassadors for our journal and the APS. [Extracted from the article]

Published
2021
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34. Impact of Cell Composition and Geometry on Human Induced Pluripotent Stem Cells-Derived Engineered Cardiac Tissue

Author

70645754, Nakane, Takeichiro, Masumoto, Hidetoshi, Tinney, Joseph P., Yuan, Fangping, Kowalski, William J., Ye, Fei, Leblanc, Amanda J., Sakata, Ryuzo, Yamashita, Jun K., Keller, Bradley B., 70645754, Nakane, Takeichiro, Masumoto, Hidetoshi, Tinney, Joseph P., Yuan, Fangping, Kowalski, William J., Ye, Fei, Leblanc, Amanda J., Sakata, Ryuzo, Yamashita, Jun K., and Keller, Bradley B.

Abstract

The current study describes a scalable, porous large-format engineered cardiac tissue (LF-ECT) composed of human induced pluripotent stem cells (hiPSCs) derived multiple lineage cardiac cells with varied 3D geometries and cell densities developed towards the goal of scale-up for large animal pre-clinical studies. We explored multiple 15 × 15 mm ECT geometries using molds with rectangular internal staggered posts (mesh, ME), without posts (plain sheet, PS), or long parallel posts (multiple linear bundles, ML) and a gel matrix containing hiPSC-derived cardiomyocytes, endothelial, and vascular mural cells matured in vitro for 14 days. ME-ECTs displayed the lowest dead cell ratio (p < 0.001) and matured into 0.5 mm diameter myofiber bundles with greater 3D cell alignment and higher active stress than PS-ECTs. Increased initial ECT cell number beyond 6 M per construct resulted in reduced cell survival and lower active stress. The 6M-ME-ECTs implanted onto 1 week post-infarct immune tolerant rat hearts engrafted, displayed evidence for host vascular coupling, and recovered myocardial structure and function with reduced scar area. We generated a larger (30 × 30 mm) ME-ECT to confirm scalability. Thus, large-format ECTs generated from hiPSC-derived cardiac cells may be feasible for large animal preclinical cardiac regeneration paradigms.

Published
2017

36. Loss of NHERF-1 expression prevents dopamine-mediated Na-K-ATPase regulation in renal proximal tubule cells from rat models of hypertension: aged F344 rats and spontaneously hypertensive rats

Author

Barati, Michelle T., primary, Ketchem, Corey J., additional, Merchant, Michael L., additional, Kusiak, Walter B., additional, Jose, Pedro A., additional, Weinman, Edward J., additional, LeBlanc, Amanda J., additional, Lederer, Eleanor D., additional, and Khundmiri, Syed J., additional

Published
2017
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40. Microvascular Repair: Post-Angiogenesis Vascular Dynamics

Author

LeBlanc, Amanda J., Krishnan, Laxminarayanan, Sullivan, Christopher J., Williams, Stuart K., and Hoying, James B.

Subjects
Microcirculation, Microvessels, Animals, Humans, Neovascularization, Physiologic, Regeneration, Article
Abstract

Vascular compromise and the accompanying perfusion deficits cause or complicate a large array of disease conditions and treatment failures. This has prompted the exploration of therapeutic strategies to repair or regenerate vasculatures thereby establishing more competent microcirculatory beds. Growing evidence indicates that an increase in vessel numbers within a tissue does not necessarily promote an increase in tissue perfusion. Effective regeneration of a microcirculation entails the integration of new stable microvessel segments into the network via neovascularization. Beginning with angiogenesis, neovascularization entails an integrated series of vascular activities leading to the formation of a new mature microcirculation and includes vascular guidance and inosculation, vessel maturation, pruning, arterio-venous specification, network patterning, structural adaptation, intussusception, and microvascular stabilization. While the generation of new vessel segments is necessary to expand a network, without the concomitant neovessel remodeling and adaptation processes intrinsic to microvascular network formation, these additional vessel segments give rise to a dysfunctional microcirculation. While many of the mechanisms regulating angiogenesis have been detailed, a thorough understanding of the mechanisms driving post-angiogenesis activities specific to neovascularization has yet to be fully realized, but is necessary in order to develop effective therapeutic strategies for repairing compromised microcirculations as a means to treat disease.

Published
2012

41. Sexual dimorphism in development of kidney damage in the aging Fischer-344 (F344) rat

Author

Sasser, Jennifer M., Akinsiku, Oladele, Moningka, Natasha C., Jerzewski, Katie, LeBlanc, Amanda J., Kang, Lori S., Sindler, Amy L., Muller-Delp, Judy M., and Baylis, Chris

Subjects
Male, Aging, Sex Characteristics, Kidney Cortex, Nitric Oxide Synthase Type III, Kidney Glomerulus, Age Factors, Nitric Oxide Synthase Type I, Nitric Oxide, Article, Rats, Inbred F344, Rats, Disease Models, Animal, Animals, Female
Abstract

Aging kidneys exhibit slowly developing injury and women are usually protected compared with men, in association with maintained renal nitric oxide.Our purpose was to test 2 hypotheses: (1) that aging intact Fischer-344 (F344) female rats exhibit less glomerular damage than similarly aged males, and (2) that loss of female ovarian hormones would lead to greater structural injury and dysregulation of the nitric oxide synthase (NOS) system in aging F344 rat kidneys.We compared renal injury in F344 rats in intact, ovariectomized, and ovariectomized with estrogen replaced young (6 month) and old (24 month) female rats with young and old intact male rats and measured renal protein abundance of NOS isoforms and oxidative stress.There was no difference in age-dependent glomerular damage between young or old intact male and female F344 rats, and neither ovariectomy nor estrogen replacement affected renal injury; however, tubulointerstitial injury was greater in old males than in old females. These data suggest that ovarian hormones do not influence these aspects of kidney aging in F344 rats and that the greater tubulointerstitial injury is caused by male sex. Old males had greater kidney cortex NOS3 abundance than females, and NOS1 abundance (alpha and beta isoforms) was increased in old males compared with both young males and old females. NOS abundance was preserved with age in intact females, ovariectomy did not reduce NOS1 or NOS3 protein abundance, and estrogen replacement did not uniformly elevate NOS proteins, suggesting that estrogens are not primary regulators of renal NOS abundance in this strain. Nicotinamide adenine dinucleotide phosphate oxidase-dependent superoxide production and nitrotyrosine immunoreactivity were increased in aging male rat kidneys compared with females, which could compromise renal nitric oxide production and/or bioavailability.The kidney damage expressed in aging F344 rats is fairly mild and is not related to loss of renal cortex NOS3 or NOS1 alpha.

Published
2012

42. Systemically Delivered Adipose Stromal Vascular Fraction Cells Disseminate to Peripheral Artery Walls and Reduce Vasomotor Tone Through a CD11b+ Cell-Dependent Mechanism

Author

Morris, Marvin E., primary, Beare, Jason E., additional, Reed, Robert M., additional, Dale, Jacob R., additional, LeBlanc, Amanda J., additional, Kaufman, Christina L., additional, Zheng, Huaiyu, additional, Ng, Chin K., additional, Williams, Stuart K., additional, and Hoying, James B., additional

Published
2015
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45. Adipose-Derived Stromal Vascular Fraction Cell Effects on a Rodent Model of Thin Endometrium.

Author

IIHunter, Robert K., Nevitt, Chris D., Gaskins, Jeremy T., Keller, Bradley B., Jr.Bohler, Henry C. L., and LeBlanc, Amanda J.

Subjects
ADIPOSE tissues, STROMAL cells, ENDOMETRIUM, ENDOMETRIAL diseases, FEMALE infertility, LABORATORY rodents, HEALTH outcome assessment, THERAPEUTICS
Abstract

Endometrial dysfunction affects approximately 1% of infertile women, and there is currently no standard therapy for improving fertility treatment outcomes in these patients. In our study, we utilized a rodent model of thin endometrium to test whether intrauterine application of adipose-derived stromal vascular fraction cells (SVF) could improve morphological and physiological markers of endometrial receptivity. Using anhydrous ethanol, endometrial area and gland density were significantly reduced in our model of thin endometrium. Application of SVF was associated with a 29% reduction in endometrial vascular endothelial growth factor (VEGF) expression and significant increases in uterine artery systolic/diastolic velocity ratios and resistance index values, suggesting reduced diastolic microvascular tone. However, no significant improvements in endometrial area or gland density were observed following SVF treatment. 3D confocal imaging demonstrated poor engraftment of SVF cells into recipient tissue, which likely contributed to the negative results of this study. We suspect modified treatment protocols utilizing adjuvant estrogen and/or tail vein cell delivery may improve SVF retention and therapeutic response in subsequent studies. SVF is an easily-obtainable cell product with regenerative capability that may have a future role in the treatment of infertile women with endometrial dysfunction. [ABSTRACT FROM AUTHOR]

Published
2015
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