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Aquaporin-5 (AQP-5)


Submandibular gland-specific inflammaging-induced hyposalivation in the male senescence-accelerated mouse prone -1 line (SAM-P1).

Aging has pronounced effects on mammalian tissues and cells, but the impacts of aging on salivary gland function are relatively unknown. This study aims to evaluate the effects of aging on submandibular gland (SMG) and parotid gland (PG) functions in the male senescence-accelerated mouse. In vivo analysis at the systemic level revealed that salivary secretion induced by pilocarpine, a muscarinic agonist, from the SMG was significantly decreased in aged mice, whereas salivary secretion from the PG was not affected. To evaluate organ-level function, the SMG was perfused with the muscarinic agonists carbachol and calcium ionophore A23187 ex vivo to induce salivary secretion, and decreased saliva production was also observed in the aged SMG. Histological analysis revealed the presence of CD4-positive lymphocytes infiltrating the aged SMG. Furthermore, real-time PCR revealed that the aged SMG exhibited accelerated cell aging, increased levels of the inflammatory cytokine interleukin-6, and decreased mRNA levels of the water channel protein aquaporin-5 (AQP5). In summary, these results demonstrate that SMG function in aged mice was diminished, and that cell senescence, chronic inflammation, and the decreased gene expression of AQP5 are the likely causes of hyposalivation in the SMG of aged mice.

MeSH Terms

  • Animals
  • Aquaporin 5
  • CD4-Positive T-Lymphocytes
  • Calcimycin
  • Calcium Ionophores
  • Carbachol
  • Cellular Senescence
  • Cholinergic Agonists
  • Down-Regulation
  • Inflammation
  • Interleukin-6
  • Male
  • Mice
  • Parotid Gland
  • Submandibular Gland
  • Treatment Outcome
  • Xerostomia


  • Aging
  • Aquaporin 5
  • Inflammaging
  • Inflammation
  • Parotid gland
  • Submandibular gland

Investigation of age-related changes in the expression of aquaporin-1 and aquaporin-5 in the salivary glands of mice.

The increased AQP5 expression associated with ageing in glands, which mainly secreted a serous solution, suggests a compensation for the decreased amount of saliva secretion associated with age progression. To investigate the change in aquaporin-1 (AQP1) and aquaporin-5 (AQP5) expression in the salivary glands in young and elder mice. Twelve female mice from the Balb/C genus (30-50 g) were used. The mice were separated into two groups: Group I had 2-month-old mice and Group II had 18-month-old mice. Salivary glands (glandula parotidea, glandula sublungualis, glandula submaxillaris) were excised and examined immunohistochemically and histopathologically. AQP1 and AQP5 expression of young and elder mice was evaluated using the H-score. A p-value less than 0.05 was considered statistically significant. Upon histopathological examination, the acini of glands were found to be atrophic in elder mice. The number and diameter of intercalated ducts were increased. Indeed, the amount of adipose tissue in the gland was increased. Upon immunohistochemical examination, both AQP1 and AQP5 levels in sublingual glands of elder mice were increased (p < 0.01 and p < 0.001, respectively). However, only AQP5 levels were increased in the parotid gland of elder mice (p < 0.01).

MeSH Terms

  • Aging
  • Animals
  • Aquaporin 1
  • Aquaporin 5
  • Female
  • Immunohistochemistry
  • Mice, Inbred BALB C
  • Salivary Glands


  • Ageing
  • aquaporins
  • mice
  • salivary glands

Combinations of differentiation markers distinguish subpopulations of alveolar epithelial cells in adult lung.

Distal lung epithelium is maintained by proliferation of alveolar type II (AT2) cells and, for some daughter AT2 cells, transdifferentiation into alveolar type I (AT1) cells. We investigated if subpopulations of alveolar epithelial cells (AEC) exist that represent various stages in transdifferentiation from AT2 to AT1 cell phenotypes in normal adult lung and if they can be identified using combinations of cell-specific markers. Immunofluorescence microscopy showed that, in distal rat and mouse lungs, ∼ 20-30% of NKX2.1( ) (or thyroid transcription factor 1( )) cells did not colocalize with pro-surfactant protein C (pro-SP-C), a highly specific AT2 cell marker. In distal rat lung, NKX2.1( ) cells coexpressed either pro-SP-C or the AT1 cell marker homeodomain only protein x (HOPX). Not all HOPX( ) cells colocalize with the AT1 cell marker aquaporin 5 (AQP5), and some AQP5( ) cells were NKX2.1( ). HOPX was expressed earlier than AQP5 during transdifferentiation in rat AEC primary culture, with robust expression of both by day 7. We speculate that NKX2.1 and pro-SP-C colocalize in AT2 cells, NKX2.1 and HOPX or AQP5 colocalize in intermediate or transitional cells, and HOPX and AQP5 are expressed without NKX2.1 in AT1 cells. These findings suggest marked heterogeneity among cells previously identified as exclusively AT1 or AT2 cells, implying the presence of subpopulations of intermediate or transitional AEC in normal adult lung.

MeSH Terms

  • Aging
  • Alveolar Epithelial Cells
  • Animals
  • Antigens, Differentiation
  • Cell Differentiation
  • Cell Transdifferentiation
  • Cells, Cultured
  • Epithelial Cells
  • Mice
  • Pulmonary Alveoli
  • Rats


  • NKX2.1
  • alveolar epithelial type I cell
  • alveolar epithelial type II cell
  • aquaporin-5
  • homeodomain only protein x
  • intermediate cells
  • transdifferentiation

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