ArticleJapanese journal of ophthalmology2014
Necessity of Smad4 for the normal development of the mouse lacrimal gland.
Article in Japanese journal of ophthalmology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Proteomic and Molecular Analysis of Viable Bone Debris From Foot and Ankle Osteotomies: Implications for Autologous Grafting.Foot & ankle orthopaedics · 2025Article
- Lacrimal gland development: From signaling interactions to regenerative medicine.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Review
- miR-205 is a critical regulator of lacrimal gland development.Developmental biology · 2017Article
- Lacrimal Gland Inflammation Deregulates Extracellular Matrix Remodeling and Alters Molecular Signature of Epithelial Stem/Progenitor Cells.Investigative ophthalmology & visual science · 2015Article
- Bone Morphogenetic Protein (BMP) signaling in development and human diseases.Genes & diseases · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSmad4, a key intracellular mediator in TGF-β signaling, plays a critical role in the normal development of many tissues/organs. However, its functional role in the development of the lacrimal gland (LG) has never been reported. The aim of this study was to investigate the role Smad4 may play in the development of LG by using Smad4 conditional knockout mice and comparing their LG changes with the LG in normal control mice.
methodsSmad4 in the LG, as well as in the lens, cornea, and ectoderm of the eyelids, was conditionally inactivated by using Pax6 promoter-driven Cre-transgenic mice. Lac Z reporter was used to visualize the developing LG by X-gal staining, and standard histologic approaches were used to reveal morphologic alterations.
resultsInactivation of Smad4 resulted in reduction in the size and number of acini in the embryonic LG and in pigment accumulation within the LG, although it did not affect the formation of the primary lacrimal bud. After birth, the LG from Smad4-mutant mice developed slowly, and pigment was observed starting from the P7 mutant LG. Thereafter, the mutant LG was considerably smaller than the normal LG and was eventually replaced by adipose tissue.
conclusionsThese results support the notion that Smad4 is essential for the normal development and maintenance of the mouse LG.
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