Timp-1 expression in skin and liver. (A) Total RNA was isolated from hairless skins of Ts-4 (Timp-1^high) or Tsa-1 (Timp-1^low) mice, which had been backcrossed with DBA/2 mice, and 5 μg RNA was analyzed on a Northern blot. RNA from a cell line (H59.NA3 Lewis lung carcinoma) served as a control for migration of endogenous Timp-1 (0.9 kb) mRNA in the Northern blots in A and B. Transgenic sense and antisense Timp-1 RNAs are larger (1.1 kb) due to the 5′ noncoding sequence from the -t r a n s c r i p t i o n a l  p r o m o t e r .  ( ;k1 ) T r a n s g e n e - p o s i t i v e  m i c e ;  ( ;k2 ) -transgene-negative (wild-type) littermates. The lower panel shows equal hybridization with 18S rRNA among the samples, indicating equal RNA loading. (B) Hepatic expression of sense (in Ts-4/DBA Timp-1^high mice) and antisense -( i n  T a - 1 / D B A  T i m p - 1^{l o w}  m i c e ) -Timp-1 RNA. Fifteen micrograms of total liver RNA was analyzed by Northern hybridization using double-stranded [α³²P]-dCTP–labeled probes specific for Timp-1 or 18S rRNA. (C) Agarose gel (1.8%) showing the 196-bp fragment of the amplified sequence of Timp-1. The positive control is the Timp-1–positive cell line H59.NA3.