Development of Exocrine Cells of the Pancreas and Parotid Gland in Rats

Takeuchi, T.; Kameya, Toru; Tsumuraya, Masaru; Sugimura, T

doi:10.1159/000198210

Cited by 11 publications

(6 citation statements)

References 18 publications

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“…The rise in serum T 4 in the Vehicle/Normal group is consistent with these figures. Fetal serum corticosterone concentration is at the adult level during the last stage of gestation, rapidly declines after birth, and increases back to the adult level between 15 and 25 days of age (Takeuchi et al,1977a,1978). Maturation of the parotid acini, as assessd by α‐amylase per unit of tissue, is delayed when the postnatal rise in either thyroid or corticosteroid hormones are surgically or chemically prevented (Takeuchi et al,1977b) and precocious when either hormone is injected at 6 to 8 days of age (Sasaki et al,1976; Takeuchi et al1978; Takuma et al,1978; Kumegawa et al,1980).…”

Section: Discussionmentioning

confidence: 99%

“…Fetal serum corticosterone concentration is at the adult level during the last stage of gestation, rapidly declines after birth, and increases back to the adult level between 15 and 25 days of age (Takeuchi et al,1977a,1978). Maturation of the parotid acini, as assessd by α‐amylase per unit of tissue, is delayed when the postnatal rise in either thyroid or corticosteroid hormones are surgically or chemically prevented (Takeuchi et al,1977b) and precocious when either hormone is injected at 6 to 8 days of age (Sasaki et al,1976; Takeuchi et al1978; Takuma et al,1978; Kumegawa et al,1980). It should be noted that there are parallel effects on general development, e.g., eye opening and tooth eruption (Bakke et al,1975; Froelich and Meserve,1982; Gamborino et al,2001) that may influence parotid acinar maturation by means of early change from liquid to solid diet (Redman,1987).…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that the hydrocortisone maintained these cells past their usual disappearance by 10 days (Takada et al,2001). Furthermore, one might speculate that the cited (Takeuchi et al,1977a,1978) adult serum corticosteroid concentration before and at birth is necessary for the differentiation of the parotid mucous cells, and the low concentration after birth is insufficient to sustain them past 8 days. Administering exogenous corticosteroid to attain adult serum levels before their disappearance thus might sustain the mucous cells for awhile.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Ikeda

Aiyama

Redman³

2007

The Anatomical Record

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Administration of thyroid hormone has been shown to accelerate the early postnatal development of the rat parotid gland, but these studies have dwelt almost entirely on biochemical changes. The objective of this study was to describe the effects of exogenous thyroid hormone on morphologic aspects of the developing parotid gland, in particular the transient appearance of scattered mucous cells in this otherwise serous gland. Pups were given a daily subcutaneous injection of thyroxine (T(4)) of 0.1, 0.5, or 5.0 microg/g body weight, vehicle only (injection control), or no injection (normal control) beginning at 4 days, and killed for the collection of blood and parotid glands at intervals through 15 days. The serum was analyzed for T(4) and the glands were examined by light and electron microscopy. The results indicated that both serum T(4) and the pace of gland development were proportional to the dose of T(4). In particular, T(4) accelerated decreases in acinar size and gland area occupied by stroma and translocation of a subset of cells with small secretory granules, deeply stained with periodic acid-Schiff, from acini to intercalated ducts. However, the chronology of mucous cell disappearance was indifferent to treatment. In addition, signs of toxicity, including slower gain in body weight and greatly increased apoptosis and vacuoles in the glands, occurred with the higher doses of T(4).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Ikeda

Aiyama

Redman³

2007

The Anatomical Record

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“…Affinity-purified anti-gp300 antiserum against the major immunoreactive band labeled these bands demonstrating their immunological relatedness to mature gp300 (data not shown). Development of the pancreas continues postnatally, and dietary adaptations also occur as the pups are weaned from mother's milk to solid rodent chow (27). Attainment of the adult Mr for gp300 occurred at about the time of weaning, suggesting a dietary influence on post-translational processing of this glycoprotein.…”

Section: Resultsmentioning

confidence: 99%

Expression of sulfated gp300 and changes in glycosylation during pancreatic development.

Lisle¹,

Isom²

1996

J Histochem Cytochem.

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The pancreatic zymogen granule membrane protein gp300 is the major sulfated glycoprotein of the mouse acinar cell and has been proposed to be an important structural component of the zymogen granule membrane. A prediction of this proposed function is that gp300 expression should be coordinately regulated with the digestive enzymes and appearance of zymogen granules during differentiation of acinar cells in fetal development. By Western blots and immunolocalization with a polyclonal antiserum to gp300, we found that gp300 protein expression paralleled expression of amylase and the appearance of zymogen granules in differentiating acinar cells. Lectin blots were performed to assess the glycoconjugate composition of gp300 during development. Using the fucose binding lectin Ulex europaeus I, we found that gp300 acquires this carbohydrate only postnatally, temporally correlated with weaning. In addition, gp300 showed complex changes during postnatal development in reactivity with the galactose binding lectin peanut agglutinin (PNA) and the sialic acid binding lectin Maackia amuresis (MAA). Levels of reactivity of PNA and MAA were reciprocal, suggesting that sialylation of galactose (which can block peanut agglutinin binding) was not constant on gp300 during development.

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“…This permits the study of factors that influence gland development via interventions applied directly to the pups, thus avoiding modifications of the effects of application via the dams. Alterations of diet and hormones have been shown to influence strongly postnatal development of rodent salivary glands (Sasaki et al 1976, Takeuchi et al 1977a,b 1978, Takuma et al 1978, Kumegawa et al 1980, Johnson 1987, Ikeda et al 2008, Inukai et al 2008). Serum thyroid hormone concentration is low in the perinatal rat, increases to twice the adult level by 16 days of age, and returns to the adult level by 30 days (Clos et al 1974, Porterfield and Hendrick 1981, Dussault et al 1982, Porterfield 1985, Farwell and Dubord-Tomasetti 1999).…”

mentioning

confidence: 99%

Exogenous thyroid hormone affects myoepithelium and proliferation in the developing rat parotid gland

Ikeda

Aiyama

Redman³

2010

Biotechnic & Histochemistry

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In the mature rat parotid gland, myoepithelial cells (MEC) invest intercalated ducts, but not acini. During postnatal development, however, these cells differentiate around both intercalated ducts and acini, then translocate to only intercalated ducts during weaning. Previously, we found that thyroxine (T4) accelerates translocation of cells with small secretory granules from acini into intercalated ducts and the number of apoptotic cells increased tremendously with high doses. We present here additional analysis of the effects of T4 on developing rat parotid gland, namely, the distribution of MEC and the proliferation of parenchymal cells. Beginning at age 4 days, pups were given daily subcutaneous injections of low, medium and high doses of T4 or vehicle or no injection. At ages 4, 7, 10 and 15 days, glands were excised and processed for light microscopy. Sections were double-immunostained with antibodies against proliferating cell nuclear antigen (PCNA) and actin, and counterstained with hematoxylin. Proliferative activity was assessed via PCNA histochemistry and MEC were identified using actin histochemistry. MEC in the T4 groups invested mostly acini at 15 days in vehicle/normal glands and mostly intercalated ducts after 10 days in the T4 groups. The proliferative activity of acinar cells and MEC in vehicle/normal glands declined progressively with age and T4 increased the rate of this decline in the MEC in a dose-dependent manner. We conclude that T4 accelerates the translocation of MEC from acini to intercalated ducts, with an important mechanism being the more rapid decline in the proliferative activity of MEC than in acinar cells in the T4 groups. Some of the decline in the proliferative activity of all cells in the high and medium dose T4 groups after 7 days may have been due to dose-related thyroxine toxicity.

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Development of Exocrine Cells of the Pancreas and Parotid Gland in Rats

Cited by 11 publications

References 18 publications

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Expression of sulfated gp300 and changes in glycosylation during pancreatic development.

Exogenous thyroid hormone affects myoepithelium and proliferation in the developing rat parotid gland

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