Development of cell surface saccharides on embryonic pancreatic cells
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Cell surface glycoconjugates in the embryonic rat pancreas differentiate uniquely for each cell type, revealing distinct developmental timelines and a common progenitor cell. This study maps plasmalemmal changes during pancreatic development.
Area of Science:
- Developmental Biology
- Cell Biology
- Glycobiology
Background:
- The embryonic pancreas undergoes complex differentiation to form distinct cell types.
- Understanding the cell surface changes is crucial for deciphering developmental pathways.
Purpose of the Study:
- To investigate the temporal and cell-specific patterns of plasmalemmal glycoconjugate differentiation in the embryonic rat pancreas.
- To identify the developmental origins of acinar, endocrine, and centroacinar cells.
Main Methods:
- Utilized a battery of seven lectin-ferritin conjugates as probes for cell surface glycoconjugates.
- Examined plasmalemmal differentiation from day 15 in utero to the early postpartum stage.
Main Results:
- Plasmalemmal glycoconjugate differentiation is temporally correlated with development and unique for each cell type.
- Adult cell surface saccharide phenotype appears early in presumptive acinar cells, preceding organelle development.
- Acinar cell plasmalemma maturation occurs post-cytodifferentiation, while endocrine cell maturation involves loss of specific receptors.
Conclusions:
- Acinar, centroacinar, and endocrine cells likely arise from a common progenitor with characteristics similar to adult centroacinar cells.
- Apical and basolateral plasmalemmal domains differentiate with acinar lumen formation, establishing distinct surface polarity.
Abstract:
Using a battery of seven lectin-ferritin conjugates as probes for cell surface glycoconjugates, we have studied the pattern of plasmalemmal differentiation of cells in the embryonic rat pancreas from day 15 in utero to the early postpartum stage. Our results indicate that differentiation of plasmalemmal glycoconjugates on acinar, endocrine, and centroacinar cells is temporally correlated with development and is unique for each cell type, as indicated by lectin-ferritin binding. Specifically, (a) expression of adult cell surface saccharide phenotype can be detected on presumptive acinar cells as early as 15 d in utero, as indicated by soybean agglutinin binding, and precedes development of intracellular organelles characteristic of mature acinar cells; (b) maturation of the plasmalemma of acinar cells is reached after intracellular cytodifferentiation is completed, as indicated by appearance of Con A and fucoselectin binding sites only at day 19 of development; conversely, maturation of the endocrine cell plasmalemma is accompanied by "loss" (masking) of ricinus communis II agglutinin receptors; and (c) binding sites for fucose lectins and for soybean agglutinin are absent on endocrine and centroacinar cells at all stages examined. We conclude that acinar, centroacinar, and endocrine cells develop from a common progenitor cell(s) whose plasmalemmal carbohydrate composition resembles most closely that of the adult centroacinar cell. Finally, appearance of acinar lumina beginning at approximately 17 d in utero is accompanied by differenetiation of apical and basolateral plasmalemmal domains of epithelial cells, as indicated by enhanced binding of several lectin-ferritin conjugates to the apical plasmalemmal, a pattern that persists from this stage through adult life.