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1.	Howard, JF Jr, et al. (author) Safety and efficacy of eculizumab in anti-acetylcholine receptor antibody-positive refractory generalised myasthenia gravis (REGAIN): a phase 3, randomised, double-blind, placebo-controlled, multicentre study 2017 In: The Lancet. Neurology. - 1474-4465. ; 16:12, s. 976-986 Journal article (peer-reviewed)
2.	Alaggio, R, et al. (author) Correction: "The 5th edition of The World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms" Leukemia. 2022 Jul;36(7):1720-1748 2023 In: Leukemia. - 1476-5551. ; 37:9, s. 1944-1951 Journal article (other academic/artistic)
3.	Utsugisawa, K, et al. (author) Candesartan prevents angiotensin II-induced facilitation of hypoxic neuronal damage through PKC delta inhibition 2005 In: Brain Research. Molecular Brain Research. - : Elsevier BV. - 0169-328X. ; 135:1-2, s. 134-140 Journal article (peer-reviewed)abstract To investigate the role of protein kinase C delta (PKC delta) in angiotensin II-induced facilitation mechanisms of hypoxic neuronal damage and whether candesartan, an AT1 receptor antagonist, can suppress these mechanisms, we performed in vitro experiments which were free from vascular components using PC12 cells under hypoxic (12 h)/reoxygenation (0-48 h) conditions. Angiotensin II apparently increased the basal expression level of PKC delta phosphorylated at Ser(643) before hypoxia, promoted the cleavage of PKC delta to its catalytic fragment, and fostered the progression of DNA fragmentation after hypoxia. Candesartan inhibited both phosphorylation and cleavage of PKC delta and suppressed the angiotensin II-induced facilitation of DNA fragmentation under hypoxic/reoxygenation conditions. However, PD123319, an AT2 receptor antagonist, influenced neither PKC delta nor the angiotensin II-induced facilitation of DNA fragmentation. Furthermore, in PC12 cells expressing the ATP-binding mutant of PKC delta (PKC delta(K376R)) acting as a dominant-negative protein, both phosphorylation and cleavage of PKC delta were attenuated and DNA fragmentation was markedly suppressed regardless of the presence of angiotensin II. These findings suggest that angiotensin II-induced facilitation of DNA fragmentation under hypoxic conditions is mediated by PKC delta, and the mechanisms can be suppressed by the candesartan mediated blockade of the AT1 receptor.

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Type of publication: journal article (3)

Type of content: peer-reviewed (2); other academic/artistic (1)

Author/Editor: Hayashi, T. (1); Lee, H. (1); Robson, A. (1); Suzuki, Y. (1); Wilson, A. (1); Brown, G. (1); show more...; Matsushita, T. (1); Suzuki, S (1); Mori, T. (1); Petersen, A. (1); Kumar, S (1); Rocha, R (1); Weiss, M. (1); Takahashi, M. (1); Yasuda, T. (1); Miller, R. (1); Gupta, R. (1); Kim, M. (1); Wang, M. (1); Yoshida, S. (1); Lu, L. (1); Maier, G. (1); Yamamoto, H. (1); Gibson, T (1); Wang, Z. (1); Garcia, R. (1); Steele, J (1); Moreau, C (1); Chapman, JR (1); Kobayashi, E (1); Berti, E. (1); Lee, J. (1); Sato, M. (1); Piehl, F (1); Harris, M. (1); Kobayashi, H. (1); Nakamura, Y. (1); Uehara, T. (1); Kramer, M. (1); Nagai, H. (1); De Rosa, A. (1); Rosenquist, R. (1); Nigro, C. (1); Suzuki, H. (1); Fujii, Y. (1); Fukuda, Y. (1); Mori, M. (1); Ogawa, M (1); Masaki, K (1); Park, S. (1); show less...

University: Karolinska Institutet (2); Lund University (1)

Language: English (3)

Research subject (UKÄ/SCB): Medical and Health Sciences (1)

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