Cell population changes during atrophy and regeneration of rat parotid gland

Burgess, Lurrine; Dardick, Irving

doi:10.1016/s1079-2104(98)90038-5

Cited by 27 publications

(24 citation statements)

References 19 publications

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“…Studies of salivary gland stem cells have reported c-Kit, Sca-1, and Musashi-1 as stem cell markers 17,[31][32][33][34][35] . There are also a number of reports mentioning that epithelial stem cells of the salivary gland duct are present in intercalated ducts 36,37) and that they are present in the duct-like structures of atrophied salivary glands 7,38) . In addition, differentiated cells are reported to participate in regeneration 38,39) .…”

Section: Discussionmentioning

confidence: 99%

Regenerative Capacity of Atrophic Submandibular Gland by Duct Ligation in Mice

Akadomari

Tanaka

Mataga

2016

J. Hard Tissue Biology.

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Function degeneracy of the salivary gland leads to reduced protection against infection and reduced physiological function of the oral cavity, considerably diminishing the patient's quality of life. However, no method of treatment has yet been established to recover the secretory capacity of the salivary gland reduced by the degeneration or disappearance of the gland tissue. Ongoing salivary gland regeneration experiments using cell transplantation aim to introduce clinical regenerative treatment for the salivary gland. Because it is essential to understand the self-regenerative capacity that remains in the recipient's salivary gland, it is essential to search for optimal conditions for transplantation and establish a salivary gland atrophy model. In this context, we performed duct ligation of the submandibular gland in groups of mice for 7-, 14-, and 21-day ligation periods, compared immunohistochemical staining using acinar cell and stem cell markers, detected apoptosis using TUNEL staining, and analyzed gene expression using RT-PCR to search for the expression of factors related to regenerative capacity that remain in the atrophic salivary gland. All 3 periods of ligation led to remarkable atrophy/disappearance of acinar cells and the dominant presence of duct-like structures. These structures expressed stem cell markers most intensively after 14 days of ligation, and double immunostaining revealed the expressions of PSCA and c-Kit that coincided with them. AQP5 expression was detected in acinar cells and the apical membrane of the intercalated ducts in the normal submandibular gland and was also detected after 21 days of ligation in the remnant acinar cells and intercalated ducts. Conversely, the number of TUNELpositive apoptotic cells in the atrophic salivary gland was highest after 7 days of ligation. These results showed that the duct-like structures that exist after ligation expressed stem cell markers and AQP5, indicating the presence of a mechanism related to the regeneration of salivary gland tissue.

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Section: Discussionmentioning

confidence: 99%

Regenerative Capacity of Atrophic Submandibular Gland by Duct Ligation in Mice

Akadomari

Tanaka

Mataga

2016

J. Hard Tissue Biology.

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“…However, acinar cells do not express the FGFR2IIIb receptor and are therefore not likely to be stimulated by ⌬N23-KGF. Differentiation from intercalated duct cells into acinar cells has been shown to occur in submandibular glands of mice [6], rats [8,33], and humans [34]. Therefore, the labeling and enhanced number of BrdU ϩ acinar cells is probably caused by proliferation and subsequent differentiation of intercalated duct cells.…”

Section: Discussionmentioning

confidence: 99%

Keratinocyte Growth Factor Prevents Radiation Damage to Salivary Glands by Expansion of the Stem/Progenitor Pool

et al. 2008

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Irradiation of salivary glands during radiotherapy treatment of patients with head and neck cancer evokes persistent hyposalivation. This results from depletion of stem cells, which renders the gland incapable of replenishing saliva to produce acinar cells. The aim of this study was to investigate whether it is possible to expand the salivary gland stem/ progenitor cell population, thereby preventing acinar cell depletion and subsequent gland dysfunction after irradiation. To induce cell proliferation, keratinocyte growth factor (⌬N23-KGF, palifermin) was administered to C57BL/6 mice for 4 days before and/or after local irradiation of salivary glands. Salivary gland vitality was quantified by in vivo saliva flow rates, morphological measurements, and a newly developed in vitro salisphere progenitor/stem cell assay. Irradiation of salivary glands led to a pronounced reduction in the stem cells of the tissues, resulting in severe hyposalivation and a reduced number of acinar cells. ⌬N23-KGF treatment for 4 days before irradiation indeed induced salivary gland stem/progenitor cell proliferation, increasing the stem and progenitor cell pool. This did not change the relative radiation sensitivity of the stem/progenitor cells, but, as a consequence, an absolute higher number of stem/ progenitor cells and acinar cells survived after radiation. Postirradiation treatment with ⌬N23-KGF also improved gland function, and this effect was much more pronounced in ⌬N23-KGF pretreated animals. Post-treatment with ⌬N23-KGF seemed to act through accelerated expansion of the pool of progenitor/stem cells that survived the irradiation treatment. Overall, our data indicate that ⌬N23-KGF is a promising drug to enhance the number of salivary gland progenitor/stem cells and consequently prevent radiationinduced hyposalivation.

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“…According to previous reports, duct cells increase and acinar cells disappear in atrophic salivary glands (Walker & Gobé 1987, Cummins et al 1994, Burgess & Dardick 1998, Scott et al 1999, Takahashi et al 2000, 2002. In the regeneration, acinar cells differentiate from duct cells remaining in the atrophied glandular tissue and then actively proliferate , Cummins et al 1994, Takahashi et al 2004a, 2005.…”

Section: Introductionmentioning

confidence: 97%