Quantification of PrPC in bovine peripheral tissues: Analysis in wild-type and PrPC-deficient cattle

Kobayashi, Shinichi; Ano, Yasuhisa; Sakudo, Akikazu; Yukawa, Masayoshi; Sigiura, Katsuaki; Manabe, Noboru; Nakayama, Hiroyuki; Onodera, Takashi

doi:10.3892/mmr_00000137

Cited by 2 publications

(1 citation statement)

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“…BrdU incorporation into myocyte DNA during the first week of life could represent myocyte proliferation or the doubling in myocyte DNA content that takes place with binucleation, which has been associated with exit from the cell cycle [25,26]. To examine these issues we first performed cell cycle (DNA content) analysis of neonatal myocytes from WT and α1G−/− neonatal mouse hearts at days 1 and 7 after birth (Fig.…”

Section: Resultsmentioning

confidence: 99%

T-type Ca2+ channels regulate the exit of cardiac myocytes from the cell cycle after birth

Wang

Gao

Kubo

et al. 2013

Journal of Molecular and Cellular Cardiology

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T-type Ca2+ channels (TTCCs) are expressed in the fetal heart and then disappear from ventricular myocytes after birth. The hypothesis examined in this study was the α1G TTCCs' influence in myocyte maturation and their rapid withdrawal from the cell cycle after birth. Methods Cardiac myocytes were isolated from neonatal and adult wild type (WT), α1G−/− and α1G over expressing (α1GDT) mice. Bromodeoxyuridine (BrdU) uptake, myocyte nucleation, cell cycle analysis, and T-type Ca2+ currents were measured. Results All myocytes were mono-nucleated at birth and 35% of WT myocytes expressed functional TTCCs. Very few neonatal myocytes had functional TTCCs in α1G−/− hearts. By the end of the first week after birth no WT or α1G−/− had functional TTCCs. During the first week after birth about 25% of WT myocytes were BrdU+ and became bi-nucleated. Significantly fewer α1G−/− myocytes became bi-nucleated and fewer of these myocytes were BrdU+. Neonatal α1G−/− myocytes were also smaller than WT. Adult WT and α1G−/− hearts were similar in size, but α1G−/− myocytes were smaller and a greater % were mono-nucleated. α1G over expressing hearts were smaller than WT but their myocytes were larger. Conclusions The studies performed show that loss of functional TTCCs is associated with bi-nucleation and myocyte withdrawal from the cell cycle. Loss of α1G TTCCs slowed the transition from mono- to bi-nucleation and resulted in an adult heart with a greater number of small cardiac myocytes. These results suggest that TTCCs are involved in the regulation of myocyte size and the exit of myocytes from the cell cycle during the first week after birth.

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Section: Resultsmentioning

confidence: 99%

T-type Ca2+ channels regulate the exit of cardiac myocytes from the cell cycle after birth

Wang

Gao

Kubo

et al. 2013

Journal of Molecular and Cellular Cardiology

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Goats naturally devoid of PrPC are resistant to scrapie

Salvesen

Espenes

Reiten

et al. 2020

Vet Res

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Prion diseases are progressive and fatal, neurodegenerative disorders described in humans and animals. According to the "protein-only" hypothesis, the normal host-encoded prion protein (PrP C) is converted into a pathological and infectious form (PrP Sc) in these diseases. Transgenic knockout models have shown that PrP C is a prerequisite for the development of prion disease. In Norwegian dairy goats, a mutation (Ter) in the prion protein gene (PRNP) effectively blocks PrP C synthesis. We inoculated 12 goats (4 PRNP +/+ , 4 PRNP +/Ter , and 4 PRNP Ter/Ter) intracerebrally with goat scrapie prions. The mean incubation time until clinical signs of prion disease was 601 days post-inoculation (dpi) in PRNP +/+ goats and 773 dpi in PRNP +/Ter goats. PrP Sc and vacuolation were similarly distributed in the central nervous system (CNS) of both groups and observed in all brain regions and segments of the spinal cord. Generally, accumulation of PrP Sc was limited in peripheral organs, but all PRNP +/+ goats and 1 of 4 PRNP +/Ter goats were positive in head lymph nodes. The four PRNP Ter/Ter goats remained healthy, without clinical signs of prion disease, and were euthanized 1260 dpi. As expected, no accumulation of PrP Sc was observed in the CNS or peripheral tissues of this group, as assessed by immunohistochemistry, enzyme immunoassay, and real-time quaking-induced conversion. Our study shows for the first time that animals devoid of PrP C due to a natural mutation do not propagate prions and are resistant to scrapie. Clinical onset of disease is delayed in heterozygous goats expressing about 50% of PrP C levels.

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Quantification of PrPC in bovine peripheral tissues: Analysis in wild-type and PrPC-deficient cattle

Abstract: Abstract. cellular PrP (PrP c ) is necessary for bovine spongiform encephalopathy (BSe) infection. The purpose of the present experiment was the quantification

Cited by 2 publications

References 24 publications

T-type Ca2+ channels regulate the exit of cardiac myocytes from the cell cycle after birth

T-type Ca2+ channels regulate the exit of cardiac myocytes from the cell cycle after birth

Goats naturally devoid of PrPC are resistant to scrapie

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