GH-DT is processed by
FUCA1 to SSEA3 glycan in BMDCs. (a) GH glycan
was colocalized with FUCA1 in BMDCs within 24 h after treatment with
GH-DT. TFR and LAMP-1 represent transferrin receptor and lysosomal-associated
membrane protein 1, respectively. Arrows indicate early endosomes
containing both FUCA1 and GH glycan. (b) The colocalization rate between
GH glycan and FUCA1 was higher than that between GH glycan and FUCA2.
45 cells per group were counted. (c) Recombinant FUCA1 digested GH
glycan with the highest activity at pH = 4.5. Addition of FUCA1 inhibitor,
fuconojirimycin (FNJ), inhibited the digestion. (d) Oxidative release
of glycan and LC–MS/MS analysis showed that FUCA1 partially
hydrolyzed GH glycan on GH-DT and (e) FUCA1 completely hydrolyzed
GH glycan on GH-peptides in vitro. (f) The presentation of SSEA3 glycan
was reduced in FUCA1 or/and FUCA2 knockdown BMDCs compared to the
negative control (NC) BMDCs. Data were analyzed by paired t tests.
(g) Oxidative release of glycans and LC–MS/MS analysis showed
that the level of digested glycans was reduced in FUCA1 knockdown
BMDCs. (h) BMDCs with knockdown of FUCA1 presented more GH glycans
on the cell surface as compared to WT BMDCs. Results in (h) are mean
± SEM (n = 3). * p < 0.05,
** p < 0.01, **** p < 0.0001.