DOI: 10.1161/01.atv.10.3.410. Roles of calcium, cyclic nucleotides, and protein kinase C in regulation of endothelial permeability.

Roles of calcium, cyclic nucleotides, and protein kinase C in regulation of endothelial permeability.

10.1161/01.atv.10.3.410

Crossref journal-article

Ovid Technologies (Wolters Kluwer Health)

Arteriosclerosis: An Official Journal of the American Heart Association, Inc. (276)

Abstract

We studied the effects of calcium, cyclic nucleotides, and protein kinase C on albumin transfer, electrical resistance, and cytoskeletal actin filaments in cultured human umbilical vein endothelial cells. The endothelial monolayer grown on collagen-treated filters markedly restricted the transfer of albumin relative to its transfer across the filter alone. Both Ca++ ionophore A23187 and ethyleneglycol tetraacetic acid disrupted the integrity of the endothelial monolayer, thereby increasing endothelial albumin transfer and decreasing electrical resistance in a concentration-dependent manner. Neither W-7, a calmodulin antagonist, nor TMB-8, an intracellular Ca++ antagonist, influenced endothelial permeability. In contrast, increases in intracellular cyclic adenosine 5'-monophosphate (AMP) and/or cyclic guanosine 5'-monophosphate (GMP) induced by dibutyryl cyclic AMP, forskolin, 3-isobutyl-1-methylxanthine, 8-bromo cyclic GMP, dibutyryl cyclic GMP, or sodium nitroprusside significantly elevated endothelial electrical resistance and inhibited albumin transfer; similar effects resulted from activation of protein kinase C by phorbol-12-myristate-13-acetate or 1-oleoyl-2-acetyl-glycerol. These substances ruffled the dense peripheral bands of F-actin without compromising the integrity of endothelial monolayer. These results suggest that calcium, cyclic nucleotides, and protein kinase C play important roles in the regulation of endothelial permeability and the maintenance of endothelial integrity.

Bibliography

Yamada, Y., Furumichi, T., Furui, H., Yokoi, T., Ito, T., Yamauchi, K., Yokota, M., Hayashi, H., & Saito, H. (1990). Roles of calcium, cyclic nucleotides, and protein kinase C in regulation of endothelial permeability. Arteriosclerosis: An Official Journal of the American Heart Association, Inc., 10(3), 410â420.

Authors 9

Y Yamada (first)
T Furumichi (additional)
H Furui (additional)
T Yokoi (additional)
T Ito (additional)
K Yamauchi (additional)
M Yokota (additional)
H Hayashi (additional)
H Saito (additional)

References 0 Referenced 48

None

Dates

Type	When
Created	14 years, 2 months ago (June 17, 2011, 3:44 p.m.)
Deposited	3 years, 5 months ago (March 17, 2022, 10:18 a.m.)
Indexed	3 months, 1 week ago (May 26, 2025, 9:05 a.m.)
Issued	35 years, 4 months ago (May 1, 1990)
Published	35 years, 4 months ago (May 1, 1990)
Published Print	35 years, 4 months ago (May 1, 1990)

Funders 0

None

BibTeX

@article{Yamada_1990, title={Roles of calcium, cyclic nucleotides, and protein kinase C in regulation of endothelial permeability.}, volume={10}, ISSN={0276-5047}, url={http://dx.doi.org/10.1161/01.atv.10.3.410}, DOI={10.1161/01.atv.10.3.410}, number={3}, journal={Arteriosclerosis: An Official Journal of the American Heart Association, Inc.}, publisher={Ovid Technologies (Wolters Kluwer Health)}, author={Yamada, Y and Furumichi, T and Furui, H and Yokoi, T and Ito, T and Yamauchi, K and Yokota, M and Hayashi, H and Saito, H}, year={1990}, month=may, pages={410–420} }

JSON

{
  "indexed": {
    "date-parts": [
      [
        2025,
        5,
        26
      ]
    ],
    "date-time": "2025-05-26T13:05:30Z",
    "timestamp": 1748264730579
  },
  "reference-count": 0,
  "publisher": "Ovid Technologies (Wolters Kluwer Health)",
  "issue": "3",
  "content-domain": {
    "domain": [],
    "crossmark-restriction": false
  },
  "published-print": {
    "date-parts": [
      [
        1990,
        5
      ]
    ]
  },
  "abstract": "<jats:p>We studied the effects of calcium, cyclic nucleotides, and protein kinase C on albumin transfer, electrical resistance, and cytoskeletal actin filaments in cultured human umbilical vein endothelial cells. The endothelial monolayer grown on collagen-treated filters markedly restricted the transfer of albumin relative to its transfer across the filter alone. Both Ca++ ionophore A23187 and ethyleneglycol tetraacetic acid disrupted the integrity of the endothelial monolayer, thereby increasing endothelial albumin transfer and decreasing electrical resistance in a concentration-dependent manner. Neither W-7, a calmodulin antagonist, nor TMB-8, an intracellular Ca++ antagonist, influenced endothelial permeability. In contrast, increases in intracellular cyclic adenosine 5'-monophosphate (AMP) and/or cyclic guanosine 5'-monophosphate (GMP) induced by dibutyryl cyclic AMP, forskolin, 3-isobutyl-1-methylxanthine, 8-bromo cyclic GMP, dibutyryl cyclic GMP, or sodium nitroprusside significantly elevated endothelial electrical resistance and inhibited albumin transfer; similar effects resulted from activation of protein kinase C by phorbol-12-myristate-13-acetate or 1-oleoyl-2-acetyl-glycerol. These substances ruffled the dense peripheral bands of F-actin without compromising the integrity of endothelial monolayer. These results suggest that calcium, cyclic nucleotides, and protein kinase C play important roles in the regulation of endothelial permeability and the maintenance of endothelial integrity.</jats:p>",
  "DOI": "10.1161/01.atv.10.3.410",
  "type": "journal-article",
  "created": {
    "date-parts": [
      [
        2011,
        6,
        17
      ]
    ],
    "date-time": "2011-06-17T19:44:19Z",
    "timestamp": 1308339859000
  },
  "page": "410-420",
  "source": "Crossref",
  "is-referenced-by-count": 48,
  "title": "Roles of calcium, cyclic nucleotides, and protein kinase C in regulation of endothelial permeability.",
  "prefix": "10.1161",
  "volume": "10",
  "author": [
    {
      "given": "Y",
      "family": "Yamada",
      "sequence": "first",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "T",
      "family": "Furumichi",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "H",
      "family": "Furui",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "T",
      "family": "Yokoi",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "T",
      "family": "Ito",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "K",
      "family": "Yamauchi",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "M",
      "family": "Yokota",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "H",
      "family": "Hayashi",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    },
    {
      "given": "H",
      "family": "Saito",
      "sequence": "additional",
      "affiliation": [
        {
          "name": "First Department of Internal Medicine, Nagoya University School of Medicine, Japan."
        }
      ]
    }
  ],
  "member": "276",
  "container-title": "Arteriosclerosis: An Official Journal of the American Heart Association, Inc.",
  "original-title": [],
  "language": "en",
  "link": [
    {
      "URL": "https://www.ahajournals.org/doi/pdf/10.1161/01.ATV.10.3.410",
      "content-type": "unspecified",
      "content-version": "vor",
      "intended-application": "similarity-checking"
    }
  ],
  "deposited": {
    "date-parts": [
      [
        2022,
        3,
        17
      ]
    ],
    "date-time": "2022-03-17T14:18:00Z",
    "timestamp": 1647526680000
  },
  "score": 1,
  "resource": {
    "primary": {
      "URL": "https://www.ahajournals.org/doi/10.1161/01.ATV.10.3.410"
    }
  },
  "subtitle": [],
  "short-title": [],
  "issued": {
    "date-parts": [
      [
        1990,
        5
      ]
    ]
  },
  "references-count": 0,
  "journal-issue": {
    "issue": "3",
    "published-print": {
      "date-parts": [
        [
          1990,
          5
        ]
      ]
    }
  },
  "alternative-id": [
    "10.1161/01.ATV.10.3.410"
  ],
  "URL": "http://dx.doi.org/10.1161/01.ATV.10.3.410",
  "relation": {},
  "ISSN": [
    "0276-5047"
  ],
  "subject": [],
  "container-title-short": "Arteriosclerosis",
  "published": {
    "date-parts": [
      [
        1990,
        5
      ]
    ]
  }
}