Regeneration in pig livers by compensatory hyperplasia induces high levels of telomerase activity.
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Regeneration in pig livers by compensatory hyperplasia induces high levels of telomerase activity. / Wege, Henning; Müller, Anett; Müller, Lars; Petri, Susan; Petersen, Jörg; Hillert, Christian.
In: Comp Hepatol, Vol. 6, 2007, p. 6.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Regeneration in pig livers by compensatory hyperplasia induces high levels of telomerase activity.
AU - Wege, Henning
AU - Müller, Anett
AU - Müller, Lars
AU - Petri, Susan
AU - Petersen, Jörg
AU - Hillert, Christian
PY - 2007
Y1 - 2007
N2 - BACKGROUND: Several highly proliferative human cells transiently activate telomerase, a ribonucleoprotein with reverse transcriptase activity, to counterbalance replication-associated telomere erosion and to increase stress resistance. Quiescent human hepatocytes exhibit very low or undetectable levels of telomerase activity. However, hepatocytes display a remarkable proliferative capability following liver injury. To investigate whether liver regeneration by compensatory hyperplasia is associated with telomerase activation, we measured telomerase activity in pig livers after 70 to 80% partial hepatectomy using a fully quantitative real-time telomeric repeat amplification protocol. In contrast to commonly studied inbred laboratory mouse strains, telomere length and telomerase activity in porcine tissues are comparable to humans. RESULTS: Following partial hepatectomy, histology revealed mitotic hepatocytes as marker for compensatory hyperplasia. As expected, there was no induction of inflammation. Telomerase activity increased significantly showing the highest levels (5-fold upregulation) in pigs treated with partial hepatectomy and hepatic decompression. Moreover, telomerase activity significantly correlated to the number of mitotic hepatocytes. CONCLUSION: Our data demonstrate telomerase activation in liver regeneration by compensatory hyperplasia in a large animal model with telomere biology comparable to humans. Telomerase activation may constitute a mechanism to protect proliferating liver cells against telomere shortening and oxidative stress.
AB - BACKGROUND: Several highly proliferative human cells transiently activate telomerase, a ribonucleoprotein with reverse transcriptase activity, to counterbalance replication-associated telomere erosion and to increase stress resistance. Quiescent human hepatocytes exhibit very low or undetectable levels of telomerase activity. However, hepatocytes display a remarkable proliferative capability following liver injury. To investigate whether liver regeneration by compensatory hyperplasia is associated with telomerase activation, we measured telomerase activity in pig livers after 70 to 80% partial hepatectomy using a fully quantitative real-time telomeric repeat amplification protocol. In contrast to commonly studied inbred laboratory mouse strains, telomere length and telomerase activity in porcine tissues are comparable to humans. RESULTS: Following partial hepatectomy, histology revealed mitotic hepatocytes as marker for compensatory hyperplasia. As expected, there was no induction of inflammation. Telomerase activity increased significantly showing the highest levels (5-fold upregulation) in pigs treated with partial hepatectomy and hepatic decompression. Moreover, telomerase activity significantly correlated to the number of mitotic hepatocytes. CONCLUSION: Our data demonstrate telomerase activation in liver regeneration by compensatory hyperplasia in a large animal model with telomere biology comparable to humans. Telomerase activation may constitute a mechanism to protect proliferating liver cells against telomere shortening and oxidative stress.
M3 - SCORING: Zeitschriftenaufsatz
VL - 6
SP - 6
ER -
