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Conventional rigid 2D substrates cause complex contractile signals in monolayers of human induced pluripotent stem cell-derived cardiomyocytes.

The Journal of physiology

Huethorst E, Mortensen P, Simitev RD, Gao H, Pohjolainen L, Talman V, Ruskoaho H, Burton FL, Gadegaard N, Smith GL.
PMID: 34761809
J Physiol. 2021 Nov 11; doi: 10.1113/JP282228. Epub 2021 Nov 11.

Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) in monolayers interact mechanically via cell-cell and cell-substrate adhesion. Spatiotemporal features of contraction were analysed in hiPSC-CM monolayers (1) attached to glass or plastic (Young's modulus (E) >1 GPa), (2) detached (substrate-free)...

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Huethorst E, Mortensen P, Simitev RD, et al. Conventional rigid 2D substrates cause complex contractile signals in monolayers of human induced pluripotent stem cell-derived cardiomyocytes. J Physiol. 2021;doi: 10.1113/JP282228.
Huethorst, E., Mortensen, P., Simitev, R. D., Gao, H., Pohjolainen, L., Talman, V., Ruskoaho, H., Burton, F. L., Gadegaard, N., & Smith, G. L. (2021). Conventional rigid 2D substrates cause complex contractile signals in monolayers of human induced pluripotent stem cell-derived cardiomyocytes. The Journal of physiology, . https://doi.org/10.1113/JP282228
Huethorst, Eline, et al. "Conventional rigid 2D substrates cause complex contractile signals in monolayers of human induced pluripotent stem cell-derived cardiomyocytes." The Journal of physiology vol. (2021). doi: https://doi.org/10.1113/JP282228
Huethorst E, Mortensen P, Simitev RD, Gao H, Pohjolainen L, Talman V, Ruskoaho H, Burton FL, Gadegaard N, Smith GL. Conventional rigid 2D substrates cause complex contractile signals in monolayers of human induced pluripotent stem cell-derived cardiomyocytes. J Physiol. 2021 Nov 11; doi: 10.1113/JP282228. Epub 2021 Nov 11. PMID: 34761809.
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Inhibition of Let-7 microRNA attenuates myocardial remodeling and improves cardiac function postinfarction in mice.

Pharmacology research & perspectives

Tolonen AM, Magga J, Szabó Z, Viitala P, Gao E, Moilanen AM, Ohukainen P, Vainio L, Koch WJ, Kerkelä R, Ruskoaho H, Serpi R.
PMID: 25505600
Pharmacol Res Perspect. 2014 Aug;2(4):e00056. doi: 10.1002/prp2.56. Epub 2014 Jun 12.

The members of lethal-7 (Let-7) microRNA (miRNA) family are involved in regulation of cell differentiation and reprogramming of somatic cells into induced pluripotent stem cells. However, their function in the heart is not known. In this study, we examined...

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Tolonen AM, Magga J, Szabó Z, et al. Inhibition of Let-7 microRNA attenuates myocardial remodeling and improves cardiac function postinfarction in mice. Pharmacol Res Perspect. 2014;2(4):e00056doi: 10.1002/prp2.56.
Tolonen, A. M., Magga, J., Szabó, Z., Viitala, P., Gao, E., Moilanen, A. M., Ohukainen, P., Vainio, L., Koch, W. J., Kerkelä, R., Ruskoaho, H., & Serpi, R. (2014). Inhibition of Let-7 microRNA attenuates myocardial remodeling and improves cardiac function postinfarction in mice. Pharmacology research & perspectives, 2(4), e00056. https://doi.org/10.1002/prp2.56
Tolonen, Anna-Maria, et al. "Inhibition of Let-7 microRNA attenuates myocardial remodeling and improves cardiac function postinfarction in mice." Pharmacology research & perspectives vol. 2,4 (2014): e00056. doi: https://doi.org/10.1002/prp2.56
Tolonen AM, Magga J, Szabó Z, Viitala P, Gao E, Moilanen AM, Ohukainen P, Vainio L, Koch WJ, Kerkelä R, Ruskoaho H, Serpi R. Inhibition of Let-7 microRNA attenuates myocardial remodeling and improves cardiac function postinfarction in mice. Pharmacol Res Perspect. 2014 Aug;2(4):e00056. doi: 10.1002/prp2.56. Epub 2014 Jun 12. PMID: 25505600; PMCID: PMC4186442.
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Inhibition of .

Journal of cardiovascular development and disease

Narumanchi S, Kalervo K, Perttunen S, Wang H, Immonen K, Kosonen R, Laine M, Ruskoaho H, Tikkanen I, Lakkisto P, Paavola J.
PMID: 30987331
J Cardiovasc Dev Dis. 2019 Apr 04;6(2). doi: 10.3390/jcdd6020016.

The

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Narumanchi S, Kalervo K, Perttunen S, et al. Inhibition of . J Cardiovasc Dev Dis. 2019;6(2)doi: 10.3390/jcdd6020016.
Narumanchi, S., Kalervo, K., Perttunen, S., Wang, H., Immonen, K., Kosonen, R., Laine, M., Ruskoaho, H., Tikkanen, I., Lakkisto, P., & Paavola, J. (2019). Inhibition of . Journal of cardiovascular development and disease, 6(2), . https://doi.org/10.3390/jcdd6020016
Narumanchi, Suneeta, et al. "Inhibition of ." Journal of cardiovascular development and disease vol. 6,2 (2019). doi: https://doi.org/10.3390/jcdd6020016
Narumanchi S, Kalervo K, Perttunen S, Wang H, Immonen K, Kosonen R, Laine M, Ruskoaho H, Tikkanen I, Lakkisto P, Paavola J. Inhibition of . J Cardiovasc Dev Dis. 2019 Apr 04;6(2). doi: 10.3390/jcdd6020016. PMID: 30987331; PMCID: PMC6617397.
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["Mini Medical School"--the basics of medicine in an open university].

Duodecim; laaketieteellinen aikakauskirja

Pekkarinen H, Hietarinta M, Ilvesmäki V, Ruskoaho H.
PMID: 12181922
Duodecim. 2001;117(19):1924-8.

No abstract available.

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Pekkarinen H, Hietarinta M, Ilvesmäki V, et al. "Minilääkis"--lääketieteen perusteita avoimessa yliopistossa. ["Mini Medical School"--the basics of medicine in an open university]. Duodecim. 2001;117(19):1924-8
Pekkarinen, H., Hietarinta, M., Ilvesmäki, V., & Ruskoaho, H. (2001). "Minilääkis"--lääketieteen perusteita avoimessa yliopistossa. ["Mini Medical School"--the basics of medicine in an open university]. Duodecim; laaketieteellinen aikakauskirja, 117(19), 1924-8.
Pekkarinen, H, et al. ""Minilääkis"--lääketieteen perusteita avoimessa yliopistossa." ["Mini Medical School"--the basics of medicine in an open university]. Duodecim; laaketieteellinen aikakauskirja vol. 117,19 (2001): 1924-8.
Pekkarinen H, Hietarinta M, Ilvesmäki V, Ruskoaho H. "Minilääkis"--lääketieteen perusteita avoimessa yliopistossa. ["Mini Medical School"--the basics of medicine in an open university]. Duodecim. 2001;117(19):1924-8. Finnish. PMID: 12181922.
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Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction.

JACC. Basic to translational science

Vainio LE, Szabó Z, Lin R, Ulvila J, Yrjölä R, Alakoski T, Piuhola J, Koch WJ, Ruskoaho H, Fouse SD, Seeley TW, Gao E, Signore P, Lipson KE, Magga J, Kerkelä R.
PMID: 30847422
JACC Basic Transl Sci. 2019 Feb 25;4(1):83-94. doi: 10.1016/j.jacbts.2018.10.007. eCollection 2019 Feb.

Myocardial infarction (MI)-induced cardiac fibrosis attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Expression of connective tissue growth factor (CTGF) is elevated in affected organs in virtually every fibrotic disorder and in the diseased human...

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Vainio LE, Szabó Z, Lin R, et al. Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction. JACC Basic Transl Sci. 2019;4(1):83-94doi: 10.1016/j.jacbts.2018.10.007.
Vainio, L. E., Szabó, Z., Lin, R., Ulvila, J., Yrjölä, R., Alakoski, T., Piuhola, J., Koch, W. J., Ruskoaho, H., Fouse, S. D., Seeley, T. W., Gao, E., Signore, P., Lipson, K. E., Magga, J., & Kerkelä, R. (2019). Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction. JACC. Basic to translational science, 4(1), 83-94. https://doi.org/10.1016/j.jacbts.2018.10.007
Vainio, Laura E, et al. "Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction." JACC. Basic to translational science vol. 4,1 (2019): 83-94. doi: https://doi.org/10.1016/j.jacbts.2018.10.007
Vainio LE, Szabó Z, Lin R, Ulvila J, Yrjölä R, Alakoski T, Piuhola J, Koch WJ, Ruskoaho H, Fouse SD, Seeley TW, Gao E, Signore P, Lipson KE, Magga J, Kerkelä R. Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction. JACC Basic Transl Sci. 2019 Feb 25;4(1):83-94. doi: 10.1016/j.jacbts.2018.10.007. eCollection 2019 Feb. PMID: 30847422; PMCID: PMC6390503.
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Endothelin-1-Independent and Angiotensin II-Independent Induction of Adrenomedullin Gene Expression.

Hypertension (Dallas, Tex. : 1979)

Romppanen H, Puhakka J, Földes G, Szokodi, Vuolteenaho O, Tokola H, Tóth M, Ruskoaho H.
PMID: 11208761
Hypertension. 2001 Jan;37(1):84-90. doi: 10.1161/01.hyp.37.1.84.

-Adrenomedullin (AM) may function as an autocrine and/or paracrine factor in the heart, but the exact mechanisms regulating cardiac AM gene expression are unknown. The aim of the present study was to characterize the precise time course of induction...

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Romppanen H, Puhakka J, Földes G, et al. Endothelin-1-Independent and Angiotensin II-Independent Induction of Adrenomedullin Gene Expression. Hypertension. 2001;37(1):84-90doi: 10.1161/01.hyp.37.1.84.
Romppanen, H., Puhakka, J., Földes, G., Szokodi, Vuolteenaho, O., Tokola, H., Tóth, M., & Ruskoaho, H. (2001). Endothelin-1-Independent and Angiotensin II-Independent Induction of Adrenomedullin Gene Expression. Hypertension (Dallas, Tex. : 1979), 37(1), 84-90. https://doi.org/10.1161/01.hyp.37.1.84
Romppanen, Hannu, et al. "Endothelin-1-Independent and Angiotensin II-Independent Induction of Adrenomedullin Gene Expression." Hypertension (Dallas, Tex. : 1979) vol. 37,1 (2001): 84-90. doi: https://doi.org/10.1161/01.hyp.37.1.84
Romppanen H, Puhakka J, Földes G, Szokodi, Vuolteenaho O, Tokola H, Tóth M, Ruskoaho H. Endothelin-1-Independent and Angiotensin II-Independent Induction of Adrenomedullin Gene Expression. Hypertension. 2001 Jan;37(1):84-90. doi: 10.1161/01.hyp.37.1.84. PMID: 11208761.
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Cholecystokinin peptide signaling is regulated by a TBX5-MEF2 axis in the heart.

Peptides

Leigh RS, Ruskoaho HJ, Kaynak BL.
PMID: 33249116
Peptides. 2021 Feb;136:170459. doi: 10.1016/j.peptides.2020.170459. Epub 2020 Nov 26.

The procholecystokinin (proCCK) gene encodes a secreted peptide known to regulate the digestive, endocrine, and nervous systems. Though recently proposed as a biomarker for heart dysfunction, its physiological role in both the embryonic and adult heart is poorly understood,...

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Leigh RS, Ruskoaho HJ, Kaynak BL. Cholecystokinin peptide signaling is regulated by a TBX5-MEF2 axis in the heart. Peptides. 2020;136:170459doi: 10.1016/j.peptides.2020.170459.
Leigh, R. S., Ruskoaho, H. J., & Kaynak, B. L. (2021). Cholecystokinin peptide signaling is regulated by a TBX5-MEF2 axis in the heart. Peptides, 136170459. https://doi.org/10.1016/j.peptides.2020.170459
Leigh, Robert S, et al. "Cholecystokinin peptide signaling is regulated by a TBX5-MEF2 axis in the heart." Peptides vol. 136 (2021): 170459. doi: https://doi.org/10.1016/j.peptides.2020.170459
Leigh RS, Ruskoaho HJ, Kaynak BL. Cholecystokinin peptide signaling is regulated by a TBX5-MEF2 axis in the heart. Peptides. 2021 Feb;136:170459. doi: 10.1016/j.peptides.2020.170459. Epub 2020 Nov 26. PMID: 33249116.
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Adrenomedullin Gene Expression in the Rat Heart is Stimulated by Acute Pressure Overload: Blunted Effect in Experimental Hypertension.

Endocrinology

Romppanen H, Marttila M, Magga J, Vuolteenaho O, Kinnunen P, Szokodi IN, Ruskoaho H.
PMID: 28199606
Endocrinology. 1997 Jun 01;138(6):2636-2639. doi: 10.1210/endo.138.6.9106.

No abstract available.

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Romppanen H, Marttila M, Magga J, et al. Adrenomedullin Gene Expression in the Rat Heart is Stimulated by Acute Pressure Overload: Blunted Effect in Experimental Hypertension. Endocrinology. 1997;138(6):2636-2639doi: 10.1210/endo.138.6.9106.
Romppanen, H., Marttila, M., Magga, J., Vuolteenaho, O., Kinnunen, P., Szokodi, I. N., & Ruskoaho, H. (1997). Adrenomedullin Gene Expression in the Rat Heart is Stimulated by Acute Pressure Overload: Blunted Effect in Experimental Hypertension. Endocrinology, 138(6), 2636-2639. https://doi.org/10.1210/endo.138.6.9106
Romppanen, Hannu, et al. "Adrenomedullin Gene Expression in the Rat Heart is Stimulated by Acute Pressure Overload: Blunted Effect in Experimental Hypertension." Endocrinology vol. 138,6 (1997): 2636-2639. doi: https://doi.org/10.1210/endo.138.6.9106
Romppanen H, Marttila M, Magga J, Vuolteenaho O, Kinnunen P, Szokodi IN, Ruskoaho H. Adrenomedullin Gene Expression in the Rat Heart is Stimulated by Acute Pressure Overload: Blunted Effect in Experimental Hypertension. Endocrinology. 1997 Jun 01;138(6):2636-2639. doi: 10.1210/endo.138.6.9106. PMID: 28199606.
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Pharmacological Protein Kinase C Modulators Reveal a Pro-hypertrophic Role for Novel Protein Kinase C Isoforms in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.

Frontiers in pharmacology

Pohjolainen L, Easton J, Solanki R, Ruskoaho H, Talman V.
PMID: 33584253
Front Pharmacol. 2021 Jan 20;11:553852. doi: 10.3389/fphar.2020.553852. eCollection 2020.

No abstract available.

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Pohjolainen L, Easton J, Solanki R, et al. Pharmacological Protein Kinase C Modulators Reveal a Pro-hypertrophic Role for Novel Protein Kinase C Isoforms in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes. Front Pharmacol. 2021;11:553852doi: 10.3389/fphar.2020.553852.
Pohjolainen, L., Easton, J., Solanki, R., Ruskoaho, H., & Talman, V. (2020). Pharmacological Protein Kinase C Modulators Reveal a Pro-hypertrophic Role for Novel Protein Kinase C Isoforms in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes. Frontiers in pharmacology, 11553852. https://doi.org/10.3389/fphar.2020.553852
Pohjolainen, Lotta, et al. "Pharmacological Protein Kinase C Modulators Reveal a Pro-hypertrophic Role for Novel Protein Kinase C Isoforms in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes." Frontiers in pharmacology vol. 11 (2020): 553852. doi: https://doi.org/10.3389/fphar.2020.553852
Pohjolainen L, Easton J, Solanki R, Ruskoaho H, Talman V. Pharmacological Protein Kinase C Modulators Reveal a Pro-hypertrophic Role for Novel Protein Kinase C Isoforms in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes. Front Pharmacol. 2021 Jan 20;11:553852. doi: 10.3389/fphar.2020.553852. eCollection 2020. PMID: 33584253; PMCID: PMC7874215.
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