Filoni S, Bernardini S, Cannata S M, D'Alessio A
Dipartimento di Biologia, Università di Roma Tor Vergata, Italy.
Dev Biol. 1997 Jul 1;187(1):13-24. doi: 10.1006/dbio.1997.8598.
In Xenopus laevis, the capacity to regenerate a new lens from the outer cornea gradually decreases between stages 50 and 58, is almost negligible during the metamorphic climax, and disappears after metamorphosis. The factors responsible for lens transdifferentiation of the outer cornea are produced by the neural retina and are located in the vitreous chamber. This decrease in the regenerative capacity may be due to: (1) a reduction of the inductive power of the retina, (2) a reduction of lens-forming competence of the outer cornea, (3) an inhibition of the lens transdifferentiation process, (4) a combination of these causes. In order to test these hypotheses, fragments of outer cornea or of outer and inner corneas joined together were isolated from early larvae, late larvae and froglets, and implanted into the eye of host larvae during the premetamorphosis or the metamorphic climax. Results from implants of outer cornea into the vitreous chamber showed that the drop in lens regeneration capacity during the metamorphic climax is not due to a decrease in the inductive power of the retinal factor and that the gradual decrease in the regenerative capacity observed between stages 50 and 58 is not related to a substantial diminution in the capacity of outer cornea cells to transdifferentiate into lens fibers. Results from implants of outer and inner corneas joined together showed that in these implants the lens transdifferentiation of the outer cornea was partially inhibited. These findings indicate that the decrease in lens regeneration is mainly due to an inhibition of the lens transdifferentiation process of the outer cornea by the inner cornea. However, even implants of cornea (multilayered epithelium and substantia propria) excised from metamorphosed animals were able to form lens fibers, although to a lesser percentage than that obtained after implantation of fragments of larval outer and inner corneas. Thus, the lens-forming competence in the corneal epithelium is still present to a certain degree even when lens regeneration capacity is lost. Several observations suggest that in the lentectomized eye of late larvae and froglets the mechanical inhibition of lens transdifferentiation process exerted by the inner cornea (or the substantia propria), due to the rapid formation of a connective barrier against the spreading of the retinal factor toward the outer cornea, has a decisive role in maintaining the phenotypic stability of the outer cornea.
在非洲爪蟾中，从外角膜再生出新晶状体的能力在第50至58阶段之间逐渐下降，在变态高峰期几乎可以忽略不计，并在变态后消失。负责外角膜晶状体转分化的因子由神经视网膜产生并位于玻璃体腔中。这种再生能力的下降可能是由于：（1）视网膜诱导能力的降低，（2）外角膜形成晶状体能力的降低，（3）晶状体转分化过程的抑制，（4）这些原因的综合作用。为了检验这些假设，从早期幼虫、晚期幼虫和幼蛙中分离出外角膜片段或连接在一起的外角膜和内角膜片段，并在变态前或变态高峰期植入宿主幼虫的眼中。将外角膜植入玻璃体腔的结果表明，变态高峰期晶状体再生能力的下降不是由于视网膜因子诱导能力的降低，并且在第50至58阶段观察到的再生能力的逐渐下降与外角膜细胞转分化为晶状体纤维的能力的显著降低无关。将外角膜和内角膜连接在一起植入的结果表明，在这些植入物中，外角膜的晶状体转分化受到部分抑制。这些发现表明，晶状体再生的下降主要是由于内角膜对外角膜晶状体转分化过程的抑制。然而，即使是从变态后的动物身上切除的角膜（多层上皮和固有层）植入物也能够形成晶状体纤维，尽管形成的百分比低于幼虫外角膜和内角膜片段植入后获得的百分比。因此，即使晶状体再生能力丧失，角膜上皮中的晶状体形成能力仍然在一定程度上存在。一些观察结果表明，在晚期幼虫和幼蛙的晶状体切除眼中，由于迅速形成结缔组织屏障以阻止视网膜因子向外角膜扩散，内角膜（或固有层）对晶状体转分化过程的机械抑制在外角膜表型稳定性的维持中起决定性作用。
