Ole Jørgen Kaasbøll

• Kaasbøll, Ole Jørgen; Gadicherla, Ashish K; Wang, Jian-Hua; Monsen, Vivi Talstad; Hagelin, Else Marie Valbjørn; Dong, Meng-Qiu & Attramadal, Håvard (2018). Connective tissue growth factor (CCN2) is a matricellular preproprotein controlled by proteolytic activation. Journal of Biological Chemistry.  ISSN 0021-9258.  293(46), s 17953- 17970 . doi: 10.1074/jbc.RA118.004559 Full text in Research Archive.
• Sokolova, Marina; Vinge, Leif Erik; Alfsnes, Katrine; Olsen, Maria Belland; Eide, Lars; Kaasbøll, Ole Jørgen; Attramadal, Håvard; Torp, May-Kristin; Fosshaug, Linn Elisabeth Lillerud; Rashidi, Azita; Lien, Egil; Finsen, Alexandra; Sandanger, Øystein; Aukrust, Pål; Ranheim, Trine & Yndestad, Arne (2017). Palmitate promotes inflammatory responses and cellular senescence in cardiac fibroblasts. Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids.  ISSN 1388-1981.  1862(2), s 234- 245 . doi: 10.1016/j.bbalip.2016.11.003
• Kaasbøll, Ole Jørgen; Moe, Ingvild Tronstad; Ahmed, Muhammad Shakil; Stang, Espen; Hagelin, Else Marie Valbjørn & Attramadal, Håvard (2016). CTGF/CCN2 postconditioning increases tolerance of murine hearts towards ischemia-reperfusion injury. PLOS ONE.  ISSN 1932-6203.  11(2) . doi: 10.1371/journal.pone.0149000
• Sandanger, Øystein; Gao, E; Ranheim, Trine; Bliksøen, Marte; Kaasbøll, Ole Jørgen; Alfsnes, Katrine; Nymo, Ståle Haugset; Rashidi, Azita; Ohm, Ingrid Kristine; Attramadal, Håvard; Aukrust, Pål; Vinge, Leif Erik & Yndestad, Arne (2016). NLRP3 inflammasome activation during myocardial ischemia reperfusion is cardioprotective. Biochemical and Biophysical Research Communications - BBRC.  ISSN 0006-291X.  469(4), s 1012- 1020 . doi: 10.1016/j.bbrc.2015.12.051
• Askevold, Erik Tandberg; Aukrust, Pål; Nymo, Ståle Haugset; Lunde, Ida Gjervold; Kaasbøll, Ole Jørgen; Aakhus, Svend; Florholmen, Geir; Ohm, Ingrid Kristine; Strand, Mari; Attramadal, Håvard; Fiane, Arnt E; Dahl, Christen Peder; Finsen, Alexandra; Vinge, Leif Erik; Christensen, Geir Arve; Yndestad, Arne; Gullestad, Lars; Latini, R; Masson, S; Tavazzi, Luigi & Ueland, Thor (2014). The cardiokine secreted Frizzled related protein 3, a modulator of Wnt-signalling, in clinical and experimental heart failure. Journal of Internal Medicine.  ISSN 0954-6820.  275(6), s 621- 630 . doi: 10.1111/joim.12175
• Gravning, Jørgen A.; Ørn, Stein; Kaasbøll, Ole Jørgen; Martinov, Vladimir Nikolkaev; Manhenke, Cord A; Dickstein, Kenneth; Edvardsen, Thor; Attramadal, Håvard & Ahmed, Muhammad Shakil (2012). Myocardial Connective Tissue Growth Factor (CCN2/CTGF) Attenuates Left Ventricular Remodeling after Myocardial Infarction. PLOS ONE.  ISSN 1932-6203.  7(12) . doi: 10.1371/journal.pone.0052120 Show summary

  Aims: Myocardial CCN2/CTGF is induced in heart failure of various etiologies. However, its role in the pathophysiology of left ventricular (LV) remodeling after myocardial infarction (MI) remains unresolved. The current study explores the role of CTGF in infarct healing and LV remodeling in an animal model and in patients admitted for acute ST-elevation MI. Methods and Results: Transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) and non-transgenic littermate controls (NLC) were subjected to permanent ligation of the left anterior descending coronary artery. Despite similar infarct size (area of infarction relative to area at risk) 24 hours after ligation of the coronary artery in Tg-CTGF and NLC mice, Tg-CTGF mice disclosed smaller area of scar tissue, smaller increase of cardiac hypertrophy, and less LV dilatation and deterioration of LV function 4 weeks after MI. Tg-CTGF mice also revealed substantially reduced mortality after MI. Remote/peri-infarct tissue of Tg-CTGF mice contained reduced numbers of leucocytes, macrophages, and cells undergoing apoptosis as compared with NLC mice. In a cohort of patients with acute ST-elevation MI (n = 42) admitted to hospital for percutaneous coronary intervention (PCI) serum-CTGF levels (s-CTGF) were monitored and related to infarct size and LV function assessed by cardiac MRI. Increase in s-CTGF levels after MI was associated with reduced infarct size and improved LV ejection fraction one year after MI, as well as attenuated levels of CRP and GDF-15. Conclusion: Increased myocardial CTGF activities after MI are associated with attenuation of LV remodeling and improved LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis.

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