scholarly journals The effects of β1 and β1+2 adrenergic receptor blockade on the exercise-induced mobilization and ex vivo expansion of virus-specific T cells: implications for cellular therapy and the anti-viral immune effects of exercise

2020 ◽  
Vol 25 (6) ◽  
pp. 993-1012
Author(s):  
Hawley E. Kunz ◽  
Nadia H. Agha ◽  
Maryam Hussain ◽  
Emily C. LaVoy ◽  
Kyle A. Smith ◽  
...  
Keyword(s):  
T Cells ◽  
Adrenergic Receptor ◽  
Cellular Therapy ◽  
Ex Vivo ◽  
Ex Vivo Expansion ◽  
Receptor Blockade ◽  
Exercise Induced ◽  
Adrenergic Receptor Blockade

Enhanced contribution of NO to exercise-induced coronary responses after α-adrenergic receptor blockade

2002 ◽  
Vol 282 (2) ◽  
pp. H508-H515 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Michel Lavallée
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
No Formation ◽  
Exercise Induced ◽  
Adrenergic Effects ◽  
Adrenergic Receptor Blockade

We hypothesized that nitric oxide (NO), in addition to β-adrenergic effects, may contribute to exercise-induced coronary responses after α-adrenergic receptor blockade. Data were analyzed as relationships between coronary sinus (CS) O2 saturation (CS O2sat) or coronary blood flow (CBF) and myocardial O2 consumption (MV˙o 2). As MV˙o 2 increased, CS O2sat fell more ( P < 0.05) after N ω-nitro-l-arginine methyl ester (l-NAME; slope = −2.9 ± 0.4 × 10−2 %saturation · μl O2 · min−1 · g−1) than before (slope = −2.1 ± 0.3 × 10−2%saturation · μl O2 · min−1 · g−1). The slope of CBF versus MV˙o 2 was not altered. After blockade of α-adrenergic receptors alone (phentolamine), CS O2sat failed to decrease as MV˙o 2 increased (slope = −0.1 ± 0.5 × 10−2 %saturation · μl O2 · min−1 · g−1).l-NAME given after phentolamine led to substantial decreases in CS O2sat ( P < 0.01) as MV˙o 2 increased (slope = −2.1 ± 0.4 × 10−2 percent saturation · μl O2 −1 · min−1 · g−1). CBF responses to exercise were smaller ( P < 0.01) after phentolamine + l-NAME (slope = 6.1 ± 0.1 × 10−3 ml/μl O2) than after phentolamine alone (slope = 6.9 ± 0.2 × 10−3 ml/μl O2). Thus a significant portion of exercise-induced coronary responses after α-adrenergic receptor blockade involves NO formation.

scholarly journals Systemic β-Adrenergic Receptor Activation Augments the ex vivo Expansion and Anti-Tumor Activity of Vγ9Vδ2 T-Cells

2020 ◽  
Vol 10 ◽  
Author(s):  
Forrest L. Baker ◽  
Austin B. Bigley ◽  
Nadia H. Agha ◽  
Charles R. Pedlar ◽  
Daniel P. O'Connor ◽  
...  
Keyword(s):  
T Cells ◽  
Adrenergic Receptor ◽  
Ex Vivo ◽  
Receptor Activation ◽  
Ex Vivo Expansion ◽  
Vγ9vδ2 T Cells ◽  
Anti Tumor Activity

β-Adrenergic receptor blockade impairs NO-dependent dilation of large coronary arteries during exercise

2003 ◽  
Vol 284 (2) ◽  
pp. H501-H510 ◽  
Author(s):  
Masaki Okajima ◽  
Masayuki Takamura ◽  
Philippe Véquaud ◽  
Robert Parent ◽  
Michel Lavallée
Keyword(s):  
Shear Stress ◽  
Coronary Arteries ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Receptor Blockade ◽  
External Diameter ◽  
No Formation ◽  
Exercise Induced ◽  
Stress Dependent ◽  
Adrenergic Receptor Blockade

Shear stress-dependent nitric oxide (NO) formation prevents immoderate vascular constriction. We examined whether shear stress-dependent NO formation limits exercise-induced coronary artery constriction after β-adrenergic receptor blockade in dogs. Control exercise led to increases ( P < 0.01) in coronary blood flow (CBF) by 38 ± 5 ml/min from 41 ± 5 ml/min and in the external diameter of epicardial coronary arteries (CD) by 0.24 ± 0.03 mm from 3.33 ± 0.20 mm. CD and shear stress were linearly related. After propranolol, CD fell ( P < 0.01) during exercise (0.08 ± 0.03 from 3.23 ± 0.19 mm), and the slope of the relationship between CD and shear stress was reduced ( P< 0.01). This slope was not further altered by the additional blockade of NO formation. In propranolol-treated resting dogs, flow-dependent effects of intracoronary adenosine to mimic exercise-induced increases in shear stress (after propranolol) led to increases ( P< 0.01) in CD (0.09 ± 0.02 from 3.68 ± 0.27 mm). Thus both shear stress-dependent NO formation and β-adrenergic receptor activation are required to cause CD dilation during exercise. Suppression of β-adrenergic receptor activation leads to impaired shear stress-dependent NO formation and allows α-adrenergic constriction to become dominant.

Effect of β-Adrenergic Receptor Blockade on Blood Flow to Collateral-Dependent Myocardium During Exercise

Circulation ◽  
1995 ◽  
Vol 91 (5) ◽  
pp. 1560-1567 ◽  
Author(s):  
Jay H. Traverse ◽  
John D. Altman ◽  
James Kinn ◽  
Dirk J. Duncker ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Adrenergic Receptor Blockade

scholarly journals Processing and Ex Vivo Expansion of Adipose Tissue-Derived Mesenchymal Stem/Stromal Cells for the Development of an Advanced Therapy Medicinal Product for Use in Humans

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1908
Author(s):  
Anna Labedz-Maslowska ◽  
Agnieszka Szkaradek ◽  
Tomasz Mierzwinski ◽  
Zbigniew Madeja ◽  
Ewa Zuba-Surma
Keyword(s):  
Adipose Tissue ◽  
Medicinal Product ◽  
Stromal Cells ◽  
Manufacturing Process ◽  
Cellular Therapy ◽  
Ex Vivo ◽  
Ex Vivo Expansion ◽  
Advanced Therapy Medicinal Product ◽  
Differentiation Potential ◽  
Advanced Therapy

Adipose tissue (AT) represents a commonly used source of mesenchymal stem/stromal cells (MSCs) whose proregenerative potential has been widely investigated in multiple clinical trials worldwide. However, the standardization of the manufacturing process of MSC-based cell therapy medicinal products in compliance with the requirements of the local authorities is obligatory and will allow us to obtain the necessary permits for product administration according to its intended use. Within the research phase (RD), we optimized the protocols used for the processing and ex vivo expansion of AT-derived MSCs (AT-MSCs) for the development of an Advanced Therapy Medicinal Product (ATMP) for use in humans. Critical process parameters (including, e.g., the concentration of enzyme used for AT digestion, cell culture conditions) were identified and examined to ensure the high quality of the final product containing AT-MSCs. We confirmed the identity of isolated AT-MSCs as MSCs and their trilineage differentiation potential according to the International Society for Cellular Therapy (ISCT) recommendations. Based on the conducted experiments, in-process quality control (QC) parameters and acceptance criteria were defined for the manufacturing of hospital exemption ATMP (HE-ATMP). Finally, we conducted a validation of the manufacturing process in a GMP facility. In the current study, we presented a process approach leading to the optimization of processing and the ex vivo expansion of AT-MSCs for the development of ATMP for use in humans.

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