Beta-Arrestins and Receptor Signaling in the Vascular Endothelium

Lee, Claudia; Viswanathan, Gayathri; Choi, Issac; Jassal, Chanpreet; Kohlmann, Taylor; Rajagopal, Sudarshan

doi:10.3390/biom11010009

Cited by 9 publications

(8 citation statements)

References 128 publications

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“…Damage to the vascular endothelium means an imbalance in vasoconstrictor and diastolic function, which is highly associated with CVDs risk factors. During lipoprotein catabolism, fatty acids are deposited on the vascular endothelium [31,32] . A high-fat diet transiently causes vascular endothelial dysfunction, which is closely related to postprandial oxidative stress.…”

Section: Protecting Vascular Endothelial Functionmentioning

confidence: 99%

Protective effects of oleic acid and polyphenols in extra virgin olive oil on cardiovascular diseases

Lu¹,

Zhao²,

Xin³

et al. 2024

Food Science and Human Wellness

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The Mediterranean diet has long been recognized as one of the most effective ways to prevent and improve cardiovascular disease. Extra virgin olive oil (EVOO) is the typical sources of fat in the Mediterranean diet which have been shown to have noteworthy nutritional value and positive impact on human health. It is worth noting that EVOO owes its superior nutritional value to its bioactive composition. The main component of EVOO is monounsaturated fatty acids (MUFAs) in the form of oleic acid. Oleic acid accounts for up to 70%-80% of EVOO. Secondly, EVOO contains approximately more than 30 phenolic compounds, of which HT is essential for the protection against CVDs. In this review, we focused on the potential mechanisms of oleic acid and polyphenols combat cardiovascular diseases risk in terms of oxidative stress, inflammation, blood pressure, endothelial function and cholesterol. This review might provide a reference for the studies on cardiovascular protective effects of EVOO.

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Section: Protecting Vascular Endothelial Functionmentioning

confidence: 99%

Protective effects of oleic acid and polyphenols in extra virgin olive oil on cardiovascular diseases

Lu¹,

Zhao²,

Xin³

et al. 2024

Food Science and Human Wellness

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“…This could serve as a cellular defense mechanism against overstimulation. [82][83][84][85]. At baseline, AngII binds to AT1R in its resting state.…”

Section: Receptor Interactions: Desensitization and Tachyphylaxismentioning

confidence: 99%

Structural Features Influencing the Bioactive Conformation of Angiotensin II and Angiotensin A: Relationship between Receptor Desensitization, Addiction, and the Blood–Brain Barrier

Moore,

Ridway,

Gadanec

et al. 2024

IJMS

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The N-terminal portion of the octapeptide angiotensin II (DRVYIHPF; AngII), a vasopressor peptide that favorably binds to, and activates, AngII type 1 receptor (AT1R), has an important role in maintaining bioactive conformation. It involves all three charged groups, namely (i) the N-terminal amino group cation, (ii) the Asp sidechain anion and (iii) the Arg guanidino cation. Neutralization of any one of these three charged groups results in a substantial reduction (<5%) in bioactivity, implicating a specialized function for this cluster. In contrast, angiotensin A (ARVYIHPF; AngA) has reduced bioactivity at AT1R; however, replacement of Asp in AngII with sarcosine (N-methyl-glycine) not only restores bioactivity but increases the activity of agonist, antagonist, and inverse agonist analogues. A bend produced at the N-terminus by the introduction of the secondary amino acid sarcosine is thought to realign the functional groups that chaperone the C-terminal portion of AngII, allowing transfer of the negative charge originating at the C-terminus to be transferred to the Tyr hydroxyl-forming tyrosinate anion, which is required to activate the receptor and desensitizes the receptor (tachyphylaxis). Peptide (sarilesin) and nonpeptide (sartans) moieties, which are long-acting inverse agonists, appear to desensitize the receptor by a mechanism analogous to tachyphylaxis. Sartans/bisartans were found to bind to alpha adrenergic receptors resulting in structure-dependent desensitization or resensitization. These considerations have provided information on the mechanisms of receptor desensitization/tolerance and insights into possible avenues for treating addiction. In this regard sartans, which appear to cross the blood–brain barrier more readily than bisartans, are the preferred drug candidates.

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“…These results demonstrated that GHI reduced the apoptosis of rBMECs via OGD, probably through the PI3K/Akt pathway. AKT signaling is associated with increased levels of various growth-stimulating factors and pro-angiogenic molecules, such as matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF) (Lee et al, 2020). Basic fibroblast growth factor (BFGF), an important mitogenic factor, plays a key role in angiogenesis (Debreczeni et al, 2021).…”

Section: Effects Of Ghi On the Expression Of Apoptosis-related Proteins In Rbmecs After Ogd-induced Injurymentioning

confidence: 99%

Guhong Injection Protects Against Apoptosis in Cerebral Ischemia by Maintaining Cerebral Microvasculature and Mitochondrial Integrity Through the PI3K/AKT Pathway

et al. 2021

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Guhong injection (GHI) can be used for the treatment of ischemic stroke. We investigated the antiapoptotic activity of GHI, its ability to repair the cerebral microvessels and mitochondria, and the PI3K/AKT signaling pathway of GHI against cerebral ischemia. Western blot and immunohistochemical analyses were used to determine the expression of cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), cytochrome c (Cyt-c), basic fibroblast growth factor (BFGF), vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), and proteins in the PI3K/AKT signaling pathway. Transmission electron microscopy and scanning electron microscopy were used to evaluate the structures of the cerebral microvasculature and cells. Hoechst 33342 staining was used to evaluate the nuclear morphology. FITC-AV/PI double staining was used to measure the antiapoptotic effects. The fluorescent dye JC-1 was used to measure mitochondrial membrane potential. The enzyme-linked immunosorbent assay (ELISA) was used to detect the activities of matrix metalloproteinase-9 (MMP-9). Biochemical assay kits were used to detect the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA). Compared with the middle cerebral artery occlusion (MCAO) group, there was decreased infarct volume and significantly improved neurological deficits in the GHI group. In addition, the expression of Bcl-2 was significantly upregulated, while the expression of Cyt-c, Bax, and cleaved caspase-3 was notably downregulated. GHI administration attenuated the pathological change and morphology of the cerebral microvasculature, and immunohistochemical staining indicated that the expressions of BFGF, VEGF, and TGF-β1 were significantly increased. The cell morphology, cell viability, cell nuclei characteristics, and mitochondrial morphology normalized following GHI treatment, which decreased the release of Cyt-c and the mitochondrial membrane potential. The levels of LDH, MMP-9, and MDA decreased, while SOD increased. Moreover, GHI administration inhibited the activation of the PI3K/AKT signaling pathway in rat brain microvascular endothelial cells (rBMECs) following oxygen/glucose deprivation (OGD) injury. Therefore, our results show that GHI administration resulted in antiapoptosis of cerebral cells and repair of cerebral microvessels and mitochondria via the PI3K/AKT signaling pathway.

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Beta-Arrestins and Receptor Signaling in the Vascular Endothelium

Cited by 9 publications

References 128 publications

Protective effects of oleic acid and polyphenols in extra virgin olive oil on cardiovascular diseases

Protective effects of oleic acid and polyphenols in extra virgin olive oil on cardiovascular diseases

Structural Features Influencing the Bioactive Conformation of Angiotensin II and Angiotensin A: Relationship between Receptor Desensitization, Addiction, and the Blood–Brain Barrier

Guhong Injection Protects Against Apoptosis in Cerebral Ischemia by Maintaining Cerebral Microvasculature and Mitochondrial Integrity Through the PI3K/AKT Pathway

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