Post‐Natal Maturation of Acinar Cells of the Guinea Pig Pancreas: An Ultrastructural Morphometric Study

Assis, Gérson Francisco de; Cestari, Tânia Mary; Sesso, Antônio; Taga, Rumio

doi:10.1046/j.1439-0264.2003.00435.x

Cited by 8 publications

(5 citation statements)

References 28 publications

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“…The acinar lumen had electron dense particles. Similar observations were also recorded in guinea pigs by De-Assis et al (2003) and in camel by Hafez and (Zaghloul, 2017). Some acinar cells were electron dense and few acinar cells were electron lucent.…”

Section: Transmission Electron Microscopysupporting

confidence: 86%

Ultrastructural Architecture Studies of Pancreas in Guinea pig

Rajathi,

Raja,

Ramakrishnan

et al. 2023

IJAR

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Background: The pancreas is an accessory organ of the digestive system and also an important endocrine organ of vertebrates that produce and release substances in the body. The pancreas has both endocrine and exocrine function. Its endocrine function is to regulate blood sugar levels by secretion of hormones like insulin, glucagon, stomatostatin and pancreatic polypeptide and an exocrine function that helps in digestion. The study was performed to document the ultrastructural details of pancreas of guinea pigs by scanning and transmission electron microscopy. Methods: Six adult healthy guinea pigs of 16-32 weeks of age (Irrespective of sex) were procured from the Department of Laboratory Animal Medicine, TANUVAS as per ethical committee approval. Animals were dissected according to standard operating procedure by using the Carbon dioxide asphyxiations as per CPCSEA norms and pancreatic pieces were utilised for SEM and TEM study. Result: Pancreas was irregular in shaped and showed splenic, ventricular and intestinal lobes. In SEM, the parenchyma was covered by the dense irregular capsule. Each lobule contained many acini which were connected by a thin, long duct with branched pattern arrangement with increasing wall thickness and diameter. In TEM, the pancreatic tissue consisted of glandular lobules comprised of acini, islets of Langerhans and connective tissue between the lobules. Numerous mitochondria and golgi complexes were also present in the acinar cell cytoplasm along with zymogen granules and rough endoplasmic reticulum. The centroacinar cells were also found. A special type of interstitial cell named telocytes and each was found with many telopodes in the exocrine part of pancreatic parenchyma. Among the four islet cell types, alpha and beta cells could be identified.

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Section: Transmission Electron Microscopysupporting

confidence: 86%

Ultrastructural Architecture Studies of Pancreas in Guinea pig

Rajathi,

Raja,

Ramakrishnan

et al. 2023

IJAR

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“…1–3,5,6 Given the importance of maturation events to a normal exocrine pancreas, we asked if activation of a single transcription factor in damaged adult acinar cells could re-establish maturation properties and cell function. To this end, we developed an inducible transgenic mouse line that expressed a myc-tagged MIST1 protein upon Cre-mediated recombination of an upstream Lox-STOP-Lox cassette ( LSL-Mist1 myc ) (Figure 1 B ).…”

Section: Resultsmentioning

confidence: 99%

“…The initial specification of the cells begins early in mouse pancreas development (~embryonic day 12.5), but final maturation, including accumulation of abundant rough endoplasmic reticulum, maximum expression of digestive enzyme transcripts, apically localized zymogen granules, and the ability to regulate exocytosis events, occurs during late embryonic and postnatal development. 1–3 A key protein involved in this maturation process is MIST1 (also known as BHLHA15), a basic helix-loop-helix transcription factor whose expression in the pancreas is restricted to acinar cells. 4,5 Embryonic Mist1 null ( Mist1 KO ) acinar cells fail to establish an apical-basal organization, fail to position zymogen granules, and fail to generate intercellular communication.…”

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confidence: 99%

Induced Mist1 Expression Promotes Remodeling of Mouse Pancreatic Acinar Cells

et al. 2012

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BACKGROUND & AIMS Early embryogenesis involves cell fate decisions that define the body axes and establish pools of progenitor cells. Development does not stop once lineages are specified; cells continue to undergo specific maturation events, and changes in gene expression patterns lead to their unique physiological functions. Secretory pancreatic acinar cells mature postnatally to synthesize large amounts of protein, polarize, and communicate with other cells. The transcription factor MIST1 is expressed by only secretory cells and regulates maturation events. MIST1-deficient acinar cells in mice do not establish apical-basal polarity, properly position zymogen granules, or communicate with adjacent cells, disrupting pancreatic function. We investigated whether MIST1 directly induces and maintains the mature phenotype of acinar cells. METHODS We analyzed the effects of Cre-mediated expression of Mist1 in adult Mist1– deficient (Mist1KO) mice. Pancreatic tissues were collected and analyzed by light and electron microscopy, immunohistochemistry, real-time polymerase chain reaction analysis, and chromatin immunoprecipitation. Primary acini were isolated from mice and analyzed in amylase secretion assays. RESULTS Induced expression of Mist1 in adult Mist1KO mice restored wild-type gene expression patterns in acinar cells. The acinar cells changed phenotypes, establishing apical-basal polarity, increasing the size of zymogen granules, reorganizing the cytoskeletal network, communicating intercellularly (by synthesizing gap junctions), and undergoing exocytosis. CONCLUSIONS The exocrine pancreas of adult mice can be remodeled by re-expression of the transcription factor MIST1. MIST1 regulates acinar cell maturation and might be used to repair damaged pancreata in patients with pancreatic disorders.

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“…Our finding that AT 2 receptors continued to be up‐regulated during the neonatal period provides additional support for the possibility that this receptor could be involved in β‐cell maturation and, in fact, neonatal up‐regulation of developmental regulating factors beyond fetal life, followed by gradual decreases in expression with maturation, has been reported previously (Kalinyak et al, ). It has also been proposed that the postnatal period may be a critical window for pancreatic acinar and islet cell maturation (de Assis et al, ; Aguayo‐Mazzucato and Bonner‐Weir, ). Given that endocrine cells undergo additional remodeling and maturation in the 2–3 weeks after birth (Habener et al, ), our observation is compatible with a close relationship between AT 2 receptor expression and the maturation of β‐cells.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II type 2 receptor regulates the development of pancreatic endocrine cells in mouse embryos

Leung

Liang

Zhao

et al. 2013

Developmental Dynamics

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Background: We previously identified a local renin-angiotensin system (RAS) regulating the differentiation of an isolated population of human pancreatic progenitor cells. Major RAS components that regulate organogenesis have been also described in embryos; however, it is not known whether a local RAS is present in the fetal pancreas. We now hypothesize that angiotensin II type 1 (AT 1 ) and type 2 (AT 2 ) receptors are expressed in mouse embryonic pancreas and involved in regulating endocrine cell development. Results: Differential expression of AT 1 and AT 2 receptors was observed in the mouse pancreata in late embryogenesis. Systemic AT 2 , but not AT 1 , receptor blockade during the second transition in pancreatic development (from embryonic day 12.0 onward) reduced the b-cell to a-cell ratio of the neonate islets, impaired their insulin secretory function and the glucose tolerance of the pups. Studies with pancreas explants ex vivo revealed regulation by AT 2 receptors of the differentiation of pancreatic progenitors into insulin-producing cells and of the proliferation of the differentiated cell, actions that did not result from reduced angiogenesis as a secondary effect of AT 2 receptor antagonism. Conclusions: These data revealed an AT 2 receptor-mediated mechanism regulating pancreatic endocrine cell development in vivo. Developmental Dynamics 243:415-427, 2014. V C 2013 Wiley Periodicals, Inc.Key words: renin-angiotensin system; fetal pancreas; islet; insulin Key findings:Differential expression of AT 1 and AT 2 receptors was identified in mouse pancreas during pancreatic development. AT 2 receptor, but not AT 1 receptor, blockade during the second transition stage of pancreatic development altered islet cell composition and impaired both insulin secretory function of neonatal islets and glucose tolerance of the pups. Pancreas explants ex vivo data showed that AT 2 receptors were essential for the differentiation of pancreatic progenitors into insulin producing cells, as well as for proliferation of the differentiated cells. No evidence was found to suggest that AT 2 receptor regulation of b-cell development is a secondary effect of angiotensin II-induced vascular endothelial growth factor-driven angiogenesis.

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Post‐Natal Maturation of Acinar Cells of the Guinea Pig Pancreas: An Ultrastructural Morphometric Study

Cited by 8 publications

References 28 publications

Ultrastructural Architecture Studies of Pancreas in Guinea pig

Ultrastructural Architecture Studies of Pancreas in Guinea pig

Induced Mist1 Expression Promotes Remodeling of Mouse Pancreatic Acinar Cells

Angiotensin II type 2 receptor regulates the development of pancreatic endocrine cells in mouse embryos

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