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Articular Cartilage Development
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
In the cartilage anlage, in presumptive areas of synovial joint development, a prominent interzone can be discerned prior to overt differentiation. In fields of joint development, Wnt5, Wnt14 (Wnt9a), and GDF5 cooperate to induce joint formation. Wnt14 is critical in determining the location of the joint in the developing skeleton; this requires the cooperation of GDF5. Under these signals, the interzone cells become flattened and change from expressing type II collagen to expressing type I collagen (Craig et al. 1987). Induction of the interzone cells is not completely understood and may have species variations (Francis-West et al. 1999). The interzone cells appear to selectively express Wnt14 (Hartmann and Tabin 2001) and act as a signaling center through expression of noggin and chordin for control of cavitation and production of the joint space (Koyama et al. 2007; Seemann et al. 2009). Noggin is critical for joint morphogenesis, as mice lacking noggin fail to produce joints (Brunet et al. 1998; Tylzanowski et al. 2006).
Modeling Neuroretinal Development and Disease in Stem Cells
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Antagonizing both Wnt and BMP signaling also seems important for eye development. Dickkopf1 (Dkk1) is a potent antagonist of canonical Wnt signaling, and mice carrying null deletions of Dkk1 lose all cranial structures anterior to the midbrain, including the eyes (Mukhopadhyay et al., 2001). Noggin (Nog), a known inhibitor of BMP signaling, is believed to play an important role in neural induction and eye field formation (Lamb et al., 1993; Zuber et al., 2003). In animal cap assays, Nog causes increased expression of many EFTFs including Pax6, Six3, Rx, Lhx2, and Optx2 (Zuber et al., 2003). In mice, Dkk1 and Nog pathways synergize to induce head formation during gastrulation by dually antagonizing Wnt and BMP signaling, acting as a head organizer (del Barco Barrantes et al., 2003); loss of one copy each of Dkk1 and Nog also results in total loss of the anterior head. Insulin-like growth factors (IGF-1) are believed to play an important role in head and eye formations (Pera et al., 2001), and it is achieved by the inhibition of canonical Wnt signaling (Richard-Parpaillon et al., 2002) via kermit2 (Gipc1), which is both an IGF receptor- and a Frizzled receptor-interacting protein (Wu et al., 2006). Recently, work using mouse embryonic stem cells (mESCs) has confirmed the importance of the PDZ domain-containing protein GIPC PDZ domain-containing family member 1 (GIPC1) (La Torre et al., 2015). They showed that the overexpression of a dominant negative form of GIPC PDZ domain-containing family member 1 (dnGIPC1), as well as the downregulation of endogenous GIPC1, is sufficient to inhibit the development of eye field cells from mESCs. Here, GIPC1 interacts directly with IGF receptor and participates in Akt1 activation. This was confirmed by experiments where the pharmacological inhibition of Akt1 phosphorylation mimicked the dnGIPC1 phenotype. After the initial formation of the eye field, Sonic hedgehog (Shh) signaling from the midline splits the eye field to form two eyes (Chiang et al., 1996). Shh has been shown to repress Pax6 expression via ventral anterior homeobox 2 (Vax-2), a homeodomain transcription factor (Li et al., 1997; Kim and Lemke, 2006). Loss of Shh in the midline results in cyclopia, the development of a single midline eye (Chiang et al., 1996). Thus, a balance largely between Wnt and BMP signaling activations/inhibitions by localized extracellular signaling centers is crucial in regulating eye field induction and morphogenesis during early stages of development.
Embryotoxic effects of Rovral® for early chicken (Gallus gallus) development
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Beatriz Mitidiero Stachissini Arcain, Maria Cláudia Gross, Danúbia Frasson Furtado, Carla Vermeulen Carvalho Grade
Ocular development starts from a signaling cascade between surface and diencephalon ectoderm, which forms the optic vesicle, in a complex process involving several signaling molecules (Zuber et al. 2003). In early embryonic stages lack of bone morphogenic protein (BMP) signaling, by overexpression of BMP binding protein noggin, as well as defective expression of microphthalmia-associated transcription factor (MITF) lead to microphthalmia (Adler and Belecky-Adams 2002), as was observed for some embryos (n = 6) treated with Rovral®. Alterations in the expression of Sox2 have also been connected to microphthalmia as well as anophthalmia, a condition detected in one embryo treated with Rovral®. Cases of microphthalmia were previously reported in other species contaminated by pesticides (Mishra and Devi 2014; Quintaneiro, Soares, and Monteiro 2018; Sabir et al. 2015; Soni et al. 2011; Yashwanth, Pamanji, and Rao 2016). Further studies are needed to determine how Rovral® affects regulation of signaling pathways leading to eye formation.
The improvement of calvarial bone healing by durable nanogel-crosslinked materials
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Pornkawee Charoenlarp, Arun Kumar Rajendran, Rie Fujihara, Taisei Kojima, Ken-ichi Nakahama, Yoshihiro Sasaki, Kazunari Akiyoshi, Masaki Takechi, Sachiko Iseki
Growth factors (GFs) are biologically active polypeptides that have also been used to improve scaffold bioactivity as a result of their ability to stimulate stem and precursor cell maintenance, proliferation, and differentiation towards specific lineages. BMP2 belongs to transforming growth factor-β (TGF-β) superfamily is considered as a potent osteoinductive growth factor for osteogenic differentiation of various stem cells. Therefore, BMP2 has been widely used for bone regeneration applications [12,13]. FGF18 is a member of the FGF family and the candidate growth factor for bone regeneration since it is involved in osteogenesis during skeletal development [14,15]. Several studies have shown that FGF18 can promote differentiation of osteoblastic cells in fetal skull bone formation by upregulating BMP2 expression, accompanied by Noggin downregulation [16,17]. However, FGF18 itself cannot accelerates bone formation in mouse calvarial bone defect model [18]. Combination of hFGF18 and hBMP2 showed enhanced and stable bone regeneration in mouse calvarial bone healing, so FGF18 activated bone regeneration only in the presence of BMP2 [18]. Therefore, co-administration of these two GFs with appropriate scaffold would be a promising strategy for bone regenerative therapy.